The AHR in the Control of Cell Cycle and Apoptosis

The AH Receptor in Biology and Toxicology

Volumn , Issue , 2011, Pages 467-483

  Dietrich, Cornelia ^a  

^a JOHANNES GUTENBERG UNIVERSITY   (Germany)

Author keywords

AHR endogenous role, apoptosis regulation; AHR in cell cycle, apoptosis control; Pleiotropic, AHR effects

Indexed keywords

EID: 84876670836     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1002/9781118140574.ch32     Document Type: Chapter

References (198)

1. Nukaya, M., Moran, S., and Bradfield, C. A. (2009). The role of the dioxin-responsive element cluster between the Cyp1a1 and Cyp1a2 loci in aryl hydrocarbon receptor biology. Proceedings of the National Academy of Sciences of the United States of America, 106, 4923-4928.
2. Uno, S., Dalton, T. P., Sinclair, P. R., Gorman, N., Wang, B., Smith, A. G., Miller, M. L., Shertzer, H. G., and Nebert, D.W. (2004). Cyp1a1(-/-)malemice: protection against high-dose TCDD-induced lethality and wasting syndrome, and resistance to intrahepatocyte lipid accumulation and uroporphyria. Toxicology and Applied Pharmacology, 196, 410-421.
3. Tuomisto, J. (2005). Does mechanistic understanding help in risk assessment: the example of dioxin. Toxicology and Applied Pharmacology, 207, S2-S10.
4. Barouki, R., Coumoul, X., and Fernandez-Salguero, P. M. (2007). The aryl hydrocarbon receptor, more than a xenobiotic-interacting protein. FEBS Letters, 581, 3608-3615.
5. Andersson, P., McGuire, J., Rubio, C., Gradin, K., Whitelaw, M. L., Pettersson, S., Hanberg, A., and Poellinger, L. (2002).A constitutively active dioxin/aryl hydrocarbon receptor induces stomach tumors. Proceedings of the National Academy of Sciences of the United States of America, 99, 9990-9995.
6. Moennikes, O., Loeppen, S., Buchmann, A., Andersson, P., Ittrich, C., Poellinger, L., and Schwarz, M. (2004). A constitutively active dioxin/aryl hydrocarbon receptor promotes hepatocarcinogenesis in mice. Cancer Research, 64, 4707-4710.
7. Fan, Y., Boivin, G. P., Knudsen, E. S., Nebert, D. W., Xia, Y., and Puga, A. (2010). The aryl hydrocarbon receptor functions as a tumor suppressor of liver carcinogenesis. Cancer Research, 70, 212-220.
8. Pitot, H. C., Goldsworthy, T., Campbell, H. A., and Poland, A. (1980). Quantitative evaluation of the promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxin of hepatocarcinogenesis from diethylnitrosamine. Cancer Research, 40, 3616-36200.
9. Wölfle, D., Münzel, P., Fischer, G., and Bock, K.-W. (1988). Altered growth control of rat hepatocytes after treatment with 3,4,3',4'-tetrachlorobiphenyl in vivo and in vitro. Carcinogenesis, 9, 919-924.
10. Wölfle, D., Becker, E., and Schmutte, C. (1993). Growth stimulation of primary rat hepatocytes by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Cell Biology and Toxicology, 9, 15-31.
11. Schrenk, D., Karger, A., Lipp, H.-P., and Bock, K.-W. (1992). 2,3,7,8-Tetrachlorodibenzo-p-dioxin and ethinylestradiol as co-mitogens in cultured rat hepatocytes. Carcinogenesis, 13, 453-456.
12. Münzel, P., Bock-Hennig, B., Schieback, S., Gschaidmeier, H., Beck-Gschaidmeier, S., and Bock, K.-W. (1996). Growth modulation of hepatocytes and rat liver epithelial cells (WB-F344) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Carcinogenesis, 17, 197-202.
13. Schrenk, D., Schäfer, S., and Bock, K.-W. (1994). 2,3,7,8-Tetrachlorodibenzo-p-dioxin as growth modulator in mouse hepatocytes with high and low affinity AhR. Carcinogenesis, 15, 27-31.
14. Dietrich, C., Faust, D., Budt, S., Moskwa, M., Kunz, A., Bock, K. W., and Oesch, F. (2002). 2,3,7,8-Tetrachlorodibenzo-pdioxin-dependent release from contact inhibition in WB-F344 cells: involvement of cyclin A. Toxicology and Applied Pharmacology, 183, 117-126.
15. Chramostová, K., Vondrácek, J., Sindlerová, L., Vojtesek, B., Kozubík, A., and Machala, M. (2004). Polycyclic aromatic hydrocarbons modulate cell proliferation in rat hepatic epithelial stem-like WB-F344 cells. Toxicology and Applied Pharmacology, 196, 136-148.
16. Vondrácek, J., Chramostová, K., Plísková, M., Bláha, L., Brack, W., Kozubík, A., and Machala, M. (2004). Induction of aryl hydrocarbon receptor-mediated and estrogen receptormediated activities, and modulation of proliferation by dinaphthofurans. Environmental Toxicology and Chemistry, 23, 2214-2220.
17. Vondrácek, J., Machala, M., Bryja, V., Chramostová, K., Krcmár, P., Dietrich, C., Hampl, A., and Kozubík, A. (2005). Aryl hydrocarbon receptor-activating polychlorinated biphenyls and their hydroxylated metabolites induce cell proliferation in contact-inhibited rat liver epithelial cells. Toxicological Sciences, 83, 53-63.
18. Zatloukalová, J., Svihálková-Sindlerová, L., Kozubík, A., Krcmár, P., Machala, M., and Vondrácek, J. (2007). ß-Naphthoflavone and 3'-methoxy-4'-nitroflavone exert ambiguous effects onAh receptor-dependent cell proliferation and gene expression in rat liver 'stem-like' cells. Biochemical Pharmacology, 73, 1622-1634.
19. Weiss, C., Faust, D., Schreck, I., Ruff, A., Farwerck, T., Melenberg, A., Schneider, S., Oesch-Bartlomowicz, B., Zatloukalová, J., Vondrácek, J., Oesch, F., and Dietrich, C. (2009). TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A. Oncogene, 27, 2198-2207.
20. Dietrich, C., Faust, D., Moskwa, M., Kunz, A., Bock, K.-W., and Oesch, F. (2003). TCDD-dependent downregulation of γ-catenin in rat liver epithelial cells (WB-F344.). International Journal of Cancer, 103, 435-439.
21. Umannová, L., Zatloukalová, J., Machala, M., Krcmár, P., Májková, Z., Hennig, B., Kozubík, A., and Vondrácek, J. (2007). Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver "stem-like" cells. Toxicological Sciences, 99, 79-89.
22. Milstone, L. and Lavigne, J. (1984). 2,3,7,8-Tetrachlorodibenzo-p-dioxin induces hyperplasia in confluent cultures of human keratinocytes. Journal of Investigative Dermatology, 82, 532-534.
23. Hébert, C. D., Cao, Q. L., and Birnbaum, L. S. (1990). Inhibition of high-density growth arrest in human squamous carcinoma cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Carcinogenesis, 11, 1335-1342.
24. Fiorito, F., Pagnini, U., De Martino, L., Montagnaro, S., Ciarcia, R., Florio, S., Pacilio, M., Fucito, A., Rossi, A., Iovane, G., and Giordano, A. (2008). 2,3,7,8-Tetrachlorodibenzo-p-dioxin increases bovine herpesvirus type-1 (BHV-1) replication in Madin-Darby bovine kidney (MDBK) cells in vitro. Journal of Cellular Biochemistry, 103, 221-233.
25. Knutson, J. C. and Poland, A. (1980). 2,3,7,8-Tetrachlorodibenzo-p-dioxin: failure to demonstrate toxicity in twentythree cultured cell types. Toxicology and Applied Pharmacology, 54, 377-383.
26. Abbott, B. D. and Birnbaum, L. S. (1990). Effects ofTCDDon embryonic ureteric epithelial EGF receptor expression and cell proliferation. Teratology, 41, 71-84.
27. Bryant, P. L., Reid, L. M., Schmid, J. E., Buckalew, A. R., and Abbott, B. D. (2001). Effects of 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) on fetal mouse urinary tract epithelium in vitro. Toxicology, 162, 23-34.
28. Abbott, B. D. and Birnbaum, L. S. (1989).TCDDalters medial epithelial cell differentiation during palatogenesis. Toxicology and Applied Pharmacology, 99, 276-286.
29. Shimba, S., Komiyama, K., Moro, I., and Tezuka, M. (2002). Overexpression of the aryl hydrocarbon receptor (AhR) accelerates the cell proliferation of A549 cells. Journal of Biochemistry, 132, 795-802.
30. Wong, P. S., Li, W., Vogel, C. F., and Matsumura, F. (2009). Characterization of MCF mammary epithelial cells overexpressing the aryl hydrocarbon receptor. BMC Cancer, 9, 234.
31. Ahn, N.-S., Hu, H., Park, J.-S., Park, J.-S., Kim, J.-S., An, S., Kong, G., Aruoma, O. I., Lee, J.-S., and Kang, K.-S. (2005). Molecular mechanisms of the 2,3,7,8-tetrachlorodibenzop-dioxin-induced inverted U-shaped dose responsiveness in anchorage independent growth and proliferation of human breast epithelial cells with stem cell characteristics. Mutation Research, 579, 189-199.
32. 3H]thymidine incorporation into rat liver deoxyribonucleic acid. Toxicology, 8, 133-146.
33. Büsser, M.-T. and Lutz, W. K. (1987). Stimulation of DNA synthesis in rat and mouse liver by various tumor promoters. Carcinogenesis, 8, 1433-1437.
34. Fox, T. R., Best, L. L., Goldsworthy, S. M., Mills, J. J., and Goldsworthy, T. L. (1993). Gene expression and cell proliferation in rat liver after 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Cancer Research, 53(10 Suppl.) 2265-2271.
35. Lucier, G.W., Tritscher, A., Goldsworthy, T., Foley, J., Clark, G., and Goldstein, J. (1991). Ovarian hormones enhance 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated increases in cell proliferation and preneoplastic foci in a two-stage model for rat hepatocarcinogenesis. Cancer Research, 51, 1391-1397.
36. Maronpot, R. R., Foley, J. F., Takahashi, K., Goldsworthy, T., Clark, G., Tritscher, A., Portier, C., and Lucier, G. (1993). Dose response for TCDD promotion of hepatocarcinogenesis in rats initiated with DEN: histologic, biochemical, and cell proliferation endpoints. Environmental Health Perspectives, 101, 634-642.
37. Tritscher, A., Clark, G., Sewall, C., Sills, R., Maronpot, R., and Lucier, G. (1995). Persistence of TCDD-induced hepatic cell proliferation and growth of enzyme altered foci after chronic exposure followed by cessation of treatment in DEN initiated female rats. Carcinogenesis, 16, 2807-2811.
38. Walker, N., Miller, B., Kohn, M., Lucier, G., and Tritscher, A. (1998). Differences in kinetics of induction and reversibility of TCDD-induced changes in cell proliferation and Cyp1A1 expression in female Sprague-Dawley rat liver. Carcinogenesis, 19, 1427-1435.
39. Wölfle, D., Münzel, P., Fischer, G., and Bock, K.-W. (1988). Altered growth of rat hepatocytes after treatment with 3,4,3',4'-tetrachlorobiphenyl in vivo and in vitro. Carcinogenesis, 9, 919-924.
40. Dewa, Y., Nishimura, J., Muguruma, M., Jin, M., Saegusa, Y., Okamura, T., Tasaki, M., Umemura, T., and Mitsumori, K. (2008). ß-Naphthoflavone enhances oxidative stress responses and the induction of preneoplastic lesions in a diethylnitrosamine-initiated hepatocarcinogenesis model in partially hepatectomized rats. Toxicology, 244, 179-189.
41. Mitchell, K. A.,Wilson, S. R., and Elferink, C. J. (2010). The activated aryl hydrocarbon receptor synergizes mitogeninduced murine liver hyperplasia. Toxicology, 276, 103-109.
42. Madhukar, B. V., Brewster, D.W., and Matsumura, F. (1984). Effects of in vivo-administered 2,3,7,8-tetrachlorodibenzop-dioxin on receptor binding of epidermal growth factor in the hepatic plasma membrane of rat, guinea pig, mouse and hamster. Proceedings of the National Academy of Sciences of the United States of America, 81, 7407-7411.
43. Enan, E., El-Sabeawy, F., Scott, M., Overstreet, J., and Lasley, B. (1998). Alterations in the growth factor signal transduction pathways and modulators of the cell cycle in endocervical cells from macaques exposed to TCDD. Toxicology and Applied Pharmacology, 151, 283-293.
44. Sorkin, A. (2001). Internalization of the epidermal growth factor receptor: role in signalling. Biochemical Society Transactions, 29(Pt 4), 480-484.
45. Sewall, C. H., Lucier, G., Tritscher, A., and Clark, G. (1993). TCDD-mediated changes in hepatic epidermal growth factor receptor may be a critical event in the hepatocarcinogenic action of TCDD. Carcinogenesis, 14, 1885-1893.
46. c-src. Journal of Biochemical Toxicology, 2, 141-154.
47. Köhle, C., Gschaidmeier, H., Lauth, D., Topell, S., Zitzer, H., and Bock, K.-W. (1999). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-mediated membrane translocation of c-Src protein kinase in liver WB-F344 cells. Archives of Toxicology, 73, 152-158.
48. Enan, E. and Matsumura, F. (1996). Identification of c-Src as the integral component of the cytosolic Ah receptor complex, transducing the signal of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) through the protein phosphorylation pathway. Biochemical Pharmacology, 52, 1599-1612.
49. Blankenship, A. and Matsumura, F. (1997). 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced activation of a protein tyrosine kinase, pp60src, in murine hepatic cytosol using a cell-free system. Molecular Pharmacology, 52, 667-675.
50. Randi, A. S., Sanchez, M. S., Alvarez, L., Cardozo, J., Pontillo, C., and Kleiman de Pisarev, D. L. (2008). Hexachlorobenzene triggers AhR translocation to the nucleus, c-Src activation and EGFR transactivation in rat liver. Toxicology Letters, 177, 116-122.
51. Park, S., Dong, B., and Matsumura, F. (2007). Rapid activation of c-Src kinase by dioxin is mediated by the Cdc37-HSP90 complex as part of Ah receptor signaling in MCF10A cells. Biochemistry, 46, 899-908.
52. Matsumura, F., Enan, E., Dunlap, D. Y., Pinkerton, K. E., and Peake, J. (1997). Altered in vivo toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in c-SRC deficient mice. Biochemical Pharmacology, 53, 1397-1404.
53. Hölper, P., Faust, D., Oesch, F., and Dietrich, C. (2005). Evaluation of the role of c-Src and ERK in TCDD-dependent release from contact inhibition in WB-F344 cells. Archives of Toxicology, 79, 201-207.
54. Vogel, C. F., Zhao,Y.,Wong, P.,Young, N. F., and Matsumura, F. (2003). The use of c-src knockout mice for the identification of the main toxic signaling pathway of TCDD to induce wasting syndrome. Journal of Biochemical and Molecular Toxicology, 17, 305-315.
55. Zeytun, A., McKallip, R. J., Fisher, M., Camacho, I., Nagarkatti, M., and Nagarkatti, P. S. (2002). Analysis of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced gene expression profile in vivo using pathway-specific cDNA arrays. Toxicology, 178, 260.
56. Frueh, F.W., Hayashibara, K. C., Brown, P. O., and Whitlock, J. P., Jr., (2001). Use of cDNA microarrays to analyze dioxininduced changes in human liver gene expression. Toxicology Letters, 122, 189-203.
57. Lin, F. H., Clark, G., Birnbaum, L. S., Lucier, G. W., and Goldstein, J. A. (1991). Influence of the Ah locus on the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the hepatic epidermal growth factor receptor. Molecular Pharmacology, 39, 307-313.
58. Choi, E. J., Toscano, D. G., Ryan, J. A., Riedel, N., and Toscano, W. A., Jr., (1991). Dioxin induces transforming growth factor-α in human keratinocytes. Journal of Biological Chemistry, 266, 9591-9597.
59. Gaido, K. W., Maness, S. C., Leonard, L. S., and Greenlee, W. F. (1992). 2,3,7,8-Tetrachlorodibenzo-p-dioxin-dependent regulation of transforming growth factors-alpha and -beta 2 expression in a human keratinocyte cell line involves both transcriptional and post-transcriptional control. Journal of Biological Chemistry, 267, 24591-24595.
60. Choi, S. S., Miller, M. A., and Harper, P. A. (2006). In utero exposure to 2,3,7, 8-tetrachlorodibenzo-p-dioxin induces amphiregulin gene expression in the developing mouse ureter. Toxicological Sciences, 94, 163-174.
61. Patel, R. D., Kim, D. J., Peters, J. M., and Perdew, G. H. (2006). The aryl hydrocarbon receptor directly regulates expression of the potent mitogen epiregulin. Toxicological Sciences, 89, 75-82.
62. Du, B., Altorki, N. K., Kopelovich, L., Subbaramaiah, K., and Dannenberg, A. J. (2005). Tobacco smoke stimulates the transcription of amphiregulin in human oral epithelial cells: evidence of a cyclic AMP-responsive element binding protein-dependent mechanism. Cancer Research, 65, 5982-5988.
63. Park, R., Kim, D. H., Kim, M. S., So, H. S., Chung, H. T., Kwon, K. B., Ryu, D. G., and Kim, B. R. (1998). Association of Shc, Cbl, Grb2, and Sos following treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin in primary rat hepatocytes. Biochemical and Biophysical Research Communication, 253, 577-581.
64. Tullis, K., Olsen, H., Bombick, D. W., Matsumura, F., and Jankun, J. (1992). TCDD causes stimulation of c-ras expression in the hepatic plasma membranes in vivo and in vitro. Journal of Biochemical Toxicology, 7, 107-116.
65. Ramakrishna, G. and Anderson, L. M. (1998). Levels and membrane localization of the c-K-ras p21 protein in lungs of mice of different genetic strains and effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and Aroclor 1254. Carcinogenesis, 19, 463-470.
66. Enan, E. and Matsumura, F. (1994). Significance of TCDDinduced changes in protein phosphorylation in the adipocyte of male guinea pigs. Journal of Biochemical Toxicology, 9, 159-170.
67. Puga, A., Maier, A., and Medvedovic, M. (2000). The transcriptional signature of dioxin in human hepatoma HepG2 cells. Biochemical Pharmacology, 60, 1129-1142.
68. Jenke, H. S., Deml, E., and Oesterle, D. (1994). C-raf expression in early rat liver tumorigenesis after promotion with polychlorinated biphenyls or phenobarbital. Xenobiotica, 24, 569-580.
69. Borlak, J. and Jenke, H. S. (2008). Cross-talk between aryl hydrocarbon receptor and mitogen-activated protein kinase signaling pathway in liver cancer through c-raf transcriptional regulation. Molecular Cancer Research, 6, 1326-1336.
70. Schwarz, M., Buchmann, A., Stinchcombe, Kalkuhl, A., and Bock, K.-W. (2000). Ah receptor ligands and tumor promotion: survival of neoplastic cells. Toxicology Letters, 112-113 869-877.
71. Ashida, H., Nagy, S., and Matsumura, F. (2000). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced changes in activities of nuclear protein kinases and phosphatases affecting DNA binding activity of c-Myc and AP-1 in the livers of guinea pigs. Biochemical Pharmacology, 59, 741-751.
72. Enan, E. and Matsumura, F. (1995). Regulation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) of the DNA binding activity of transcriptional factors via nuclear protein phosphorylation in guinea pig adipose tissue. Biochemical Pharmacology, 50, 1199-1206.
73. Enan, E., El-Sabeawy, F., Scott, M., Overstreet, J., and Lasley, B. (1998). Alterations in the growth factor signal transduction pathways and modulators of the cell cycle in endocervical cells from macaques exposed to TCDD. Toxicology and Applied Pharmacology, 151, 283-293.
74. Dere, E., Boverhof, D. R., Burgoon, L. D., and Zacharewski, T. R. (2006). In vivo-in vitro toxicogenomic comparison of TCDD-elicited gene expression in Hepa1c1c7 mouse hepatoma cells and C57BL/6 hepatic tissue. BMC Genomics, 7, 80.
75. Tang, N. J., Liu, J., Coenraads, P. J., Dong, L., Zhao, L. J., Ma, S.W., Chen, X., Zhang, C. M., Ma, X. M.,Wei,W. G., Zhang, P., and Bai, Z. P. (2008). Expression of AhR, CYP1A1, GSTA1, c-fos and TGF-alpha in skin lesions from dioxinexposed humans with chloracne. Toxicology Letters, 177, 182-187.
76. Puga, A., Nebert, D.W., and Carrier, F. (1992). Dioxin induces expression of c-fos and c-jun proto-oncogenes and a large increase in transcription factor AP-1. DNA and Cell Biology, 11, 269-281.
77. Puga, A., Barnes, S. J., Chang, C., Zhu, H., Nephew, K. P., Khan, S. A., and Shertzer, H. G. (2000). Activation of transcription factors activator protein-1 and nuclear factorkappaB by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Biochemical Pharmacology, 59, 997-1005.
78. Weiss, C., Faust, D., Dürk, H., Kolluri, S. K., Pelzer, A., Schneider, S., Dietrich, C., Oesch, F., and Göttlicher, M. (2005). TCDD induces c-jun expression via a novel Ah (dioxin) receptor-mediated p38-MAPK-dependent pathway. Oncogene, 24, 4975-4983.
79. Andrysik, Z., Vondrácek, J., Machala, M, Krcmár, P., Svihálková-Sindlerová, L., Kranz, A., Weiss, C., Faust, D., Kozubík, A., and Dietrich, C. (2007). The aryl hydrocarbon receptor-dependent deregulation of cell cycle control induced by polycyclic aromatic hydrocarbons in rat liver epithelial cells. Mutation Research, 615, 87-97.
80. Gohl, G., Lehmköster, T.,Münzel, P., Schrenk, D. Viebahmn, R., and Bock, K.-W. (1996). TCDD-inducible plasminogen activator inhibitor type 2 (PAI-2) in human hepatocytes, HepG2 and monocytic U937 cells. Carcinogenesis, 17, 443-449.
81. Gierthy, J. F. and Crane, D. (1984). Reversible inhibition of in vitro epithelial cell proliferation by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicology and Applied Pharmacology, 74, 91-98.
82. Hushka, D. R. and Greenlee,W. F. (1995). 2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits DNA synthesis in rat primary hepatocytes. Mutation Research, 333, 89-99.
83. Göttlicher, M., Cikryt, P., and Wiebel, F. J. (1990). Inhibition of growth by 2,3,7,8-tetrachlorodibenzo-p-dioxin in 5L rat hepatoma cells is associated with the presence of Ah receptor. Carcinogenesis, 11, 2205-2210.
84. Weiss, C., Kolluri, S. K., Kiefer, F., and Göttlicher,M. (1996). Complementation of Ah receptor deficiency in hepatoma cells: negative feedback regulation and cell cycle control by the Ah receptor. Experimental Cell Research, 226, 154-163.
85. Morris, D. L., Karras, J. G., and Holsapple, M. P. (1993). Direct effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on responses to lipopolysaccharide (LPS) by isolated murine B-cells. Immunopharmacology, 26, 105-112.
86. Latchney, S. E., Lioy, D. T., Henry, E. C., Gasiewicz, T. S., Strathmann, F. G., Mayer-Proschel, M., and Opanashuk, L. A. (2011). Neural precursor cell proliferation is disrupted through activation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Stem Cells and Development, 20, 313-326.
87. Jin, D. Q., Jung, J. W., Lee, Y. S., and Kim, J. A. (2004). 2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits cell proliferation through aryl hydrocarbon receptor-mediated G1-arrest in SK-N-SH human neuronal cells. Neuroscience Letters, 363, 69-72.
88. Liu, H., Biegel, L., Narasimhan, T. R., Rowlands, C., and Safe, S. (1992). Inhibition of insulin-like growth factor-I responses in MCF-7 cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds. Molecular and Cellular Endocrinology, 87, 19-28.
89. Liu, H. and Safe, S. (1996). Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on insulin-induced responses in MCF-7 human breast cancer cells. Toxicology and Applied Pharmacology, 138, 242-250.
90. Kip1 induction and inhibition of proliferation by the intracellular Ah receptor in developing thymus and hepatoma cells. Genes & Development, 13, 1742-1753.
91. Lai, Z. W., Fiore, N. C., Hahn, P. J., Gasiewicz, T. A., and Silverstone, A. E. (2000). Differential effects of diethylstilbestrol and 2,3,7,8-tetrachlorodibenzo-p-dioxin on thymocyte differentiation, proliferation, and apoptosis in bcl-2 transgenic mouse fetal thymus organ culture. Toxicology and Applied Pharmacology, 168, 15-24.
92. McMillan, B. J., McMillan, S. N., Glover, E., and Bradfield C. A. (2007). 2,3,7,8-Tetrachlorodibenzo-p-dioxin induces premature activation of the KLF2 regulon during thymocyte development. Journal of Biological Chemistry, 282, 12590-12597.
93. Laiosa, M. D., Wyman, A., Murante, F. G., Fiore, N. C., Staples, J. E., Gasiewicz, T. A., and Silverstone, A. E. (2003). Cell proliferation arrestwithin intrathymic lymphocyte progenitor cells causes thymic atrophy mediated by the aryl hydrocarbon receptor. Journal of Immunology, 171, 4582-4591.
94. Laiosa, M. D., Mills, J. H., Lai, Z.W., Singh, K. P., Middleton, F. A., Gasiewicz, T. A., and Silverstone, K. E., (2010). Identification of stage-specific gene modulation during early thymocyte development by whole-genome profiling analysis after aryl hydrocarbon receptor activation. Molecular Pharmacology, 77, 773-783.
95. Ito, T., Tsukumo, S., Suzuki, N., Motohashi, H., Yamamoto, M., Fujii-Kuriyama,Y., Mimura, J., Lin, T. M., Peterson, R. E., Tohyama, C., and Nohara, K. (2004). A constitutively active arylhydrocarbon receptor induces growth inhibition of Jurkat T cells through changes in the expression of genes related to apoptosis and cell cycle arrest. Journal of Biological Chemistry, 279, 25204-25210.
96. Peng, T. L., Chen, J., Mao, W., Liu, X., Tao, Y., Chen, L. Z., and Chen, M. H. (2009). Potential therapeutic significance of increased expression of aryl hydrocarbon receptor in human gastric cancer. World Journal of Gastroenterology, 15, 1719-1729.
97. Castro-Rivera, E.,Wormke, M., and Safe, S. (1999). Estrogen and aryl hydrocarbon responsiveness of ECC-1 endometrial cancer cells. Molecular and Cellular Endocrinology, 150, 11-21.
98. Barnes-Ellerbe, S., Knudsen, K. E., and Puga, A. (2004). 2,3,7,8-Tetrachlorodibenzo-p-dioxin blocks androgendependent cell proliferation of LNCaP cells through modulation of pRB phosphorylation. Molecular Pharmacology, 66, 502-511.
99. Morrow, D., Quin, C., Smith, R., 3rd, and Safe, S. (2004). Aryl hydrocarbon receptor-mediated inhibition of LNCaP prostate cancer cell growth and hormone-induced transactivation. Journal of Steroid Biochemistry and Molecular Biology, 88, 27-36.
100. Koliopanos, A., Kleeff, J., Xiao,Y., Safe, S., Zimmermann, A., Büchler, M. W., and Friess, H. (2002). Increased arylhydrocarbon receptor expression offers a potential therapeutic target for pancreatic cancer. Oncogene, 21, 6059-6070.
101. Bauman, J.W., Goldsworthy, T. L., Dunn, C. S., and Fox, T. R. (1995). Inhibitory effects of 2,3,7,8-tetrachlorodibenzop-dioxin on rat hepatocyte proliferation induced by 2/3 partial hepatectomy. Cell Proliferation, 28, 437-451.
102. Mitchell, K. A., Lockhart, C. A., Huang, G., and Elferink, C. J. (2006). Sustained aryl hydrocarbon receptor activity attenuates liver regeneration. Molecular Pharmacology, 70, 163-170.
103. Buchmann, A., Stinchcombe, S., Körner,W., Hagenmaier, H., and Bock, K. W. (1994). Effects of 2,3,7,8-tetrachloro-and 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin on the proliferation of preneoplastic liver cells in the rat. Carcinogenesis, 15, 1143-1150.
104. Stinchcombe, S., Buchmann, A., Bock, K. W., and Schwarz, M. (1995). Inhibition of apoptosis during 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated tumour promotion in rat liver. Carcinogenesis, 16, 1271-1275.
105. Thackaberry, E. A., Jiang, Z., Johnson, C. D., Ramos, K. S., and Walker, M. K. (2005). Toxicogenomic profile of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the murine fetal heart: modulation of cell cycle and extracellular matrix genes. Toxicological Sciences, 88, 231-241.
106. Thackaberry, E. A., Nunez, B. A., Ivnitski-Steele, I. D., Friggins, M., and Walker, M. K. (2005). Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on murine heart development: alteration in fetal and postnatal cardiac growth, and postnatal cardiac chronotropy. Toxicological Sciences, 88, 242-249.
107. Lew, B. J., Collins, L. L., O'Reilly,M. A., and Lawrence, B. P. (2009). Activation of the aryl hydrocarbon receptor during different critical windows in pregnancy alters mammary epithelial cell proliferation and differentiation. Toxicological Sciences, 111, 151-162.
108. Huang, G. and Elferink, C. E. (2005). Multiple mechanisms are involved in Ah receptor-mediated cell cycle arrest. Molecular Pharmacology, 67, 88-96.
109. Marlowe, J., Knudsen, E. S., Schwemberger, S., and Puga A. (2004). The aryl hydrocarbon receptor displaces p300 from E2F-dependent promoters and represses S phase-specific gene expression. Journal of Biological Chemistry, 279, 29013-29022.
110. Ge, N.-L. and Elferink, C. E. (1998). A direct interaction between the aryl hydrocarbon receptor and the retinoblastoma protein. Journal of Biological Chemistry, 273, 22708-22713.
111. Puga, A., Barnes, S. J., Dalton, T. P., Chang, C., Knudsen, E. S., and Maier, M. A. (2000). Aromatic hydrocarbon receptor interaction with the retinoblastoma protein potentiates repression of E2F-dependent transcription and cell cycle arrest. Journal of Biological Chemistry, 275, 2943-2950.
112. Rininger, J. A., Stoffregen, D. A., and Babish, J. G. (1997). Murine hepatic p53, RB, and CDK inhibitory protein expression following acute 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. Chemosphere, 34, 1557-1568.
113. Cobrinik, D. (2005). Pocket proteins and cell cycle control. Oncogene, 24, 2796-2809.
114. Pang, P. H., Lin, Y. H., Lee, Y. H., Hou, H. H., Hsu, S. P., and Juan, S. H. (2008). Molecular mechanisms of p21 and p27 induction by 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, involved in antiproliferation of human umbilical vascular endothelial cells. Journal of Cellular Physiology, 215, 161-171.
115. Higa, L. A.,Yang, X., Zheng, J., Banks, D.,Wu, M., Ghosh, P., Sun, H., and Zhang, H. (2006). Involvement of CUL4 ubiquitin E3 ligases in regulating CDK inhibitors Dacapo/p27Kip1 and cyclin E degradation. Cell Cycle, 5, 71-77.
116. Vogel, C. and Abel, J. (1995). Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on growth factor expression in the human breast cancer cell line MCF-7. Archives of Toxicology, 69, 259-265.
117. Biegel, L. and Safe, S. (1990). Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on cell growth and the secretion of the estrogen-induced 34-,52-and 160-kDa proteins in human breast cancer cells. Journal of Steroid Biochemistry and Molecular Biology, 37, 725-732.
118. Chaloupa, K., Krishnan, V., and Safe, S. (1992). Polynuclear aromatic hydrocarbon carcinogens as anti-estrogens in MCF-7 human breast cancer cells: role of the Ah receptor. Carcinogenesis, 13, 2233-2239.
119. Zacharewski, T., Harris, M., Biegel, L., Morrison, V., Merchant, M., and Safe, S. (1992). 6-Methyl-1,3,8-trichlorodibenzofuran (MCDF) as an antiestrogen in human and rodent cancer cell lines: evidence for the role of the Ah receptor. Toxicology and Applied Pharmacology, 113, 311-318.
120. Fernandez, P. and Safe, S. (1992). Growth inhibitory and antimitogenic activity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in T47D human breast cancer cells. Toxicology Letters, 61, 185-197.
121. Liu, H.,Wormke, M., Safe, S. H., and Bjeldanes, L. F. (1994). Indolo[3,2-b]carbazole: a dietary-derived factor that exhibits both antiestrogenic and estrogenic activity. Journal of the National Cancer Institute, 86, 1758-1765.
122. Chen, I., McDougal, A., Wang, F., and Safe, S. (1998). Aryl hydrocarbon receptor-mediated anti-estrogenic and antitumorigenic activity of diindolylmethane. Carcinogenesis, 19, 1631-1639.
123. Oenga, G. N., Spink, D. C., and Carpenter, D. O. (2004). TCDD and PCBs inhibit breast cancer cell proliferation in vitro. Toxicology In Vitro, 18, 811-819.
124. Köhle, C., Hassepass, I., Bock-Hennig, B. S., Bock, K.-W., Poellinger, L., and McGuire, J. (2002). Conditional expression of a constitutively active aryl hydrocarbon receptor in MCF-7 human breast cancer cells. Archives of Biochemistry and Biophysics, 402, 172-179.
125. Merchant, M., Krishnan, V., and Safe, S. (1993). Mechanism of action of alpha-naphthoflavone as an Ah receptor antagonist in MCF-7 human breast cancer cells. Toxicology and Applied Pharmacology, 120, 179-185.
126. Abdelrahim, M., Smith, R., 3rd, and Safe, S. (2003). Aryl hydrocarbon receptor gene silencing with small inhibitory RNA differentially modulates Ah-responsiveness in MCF-7 and HepG2 cancer cells. Molecular Pharmacology, 63, 1373-1381.
127. Wang, W., Smith, R., 3rd, and Safe, S. (1998). Aryl hydrocarbon receptor-mediated antiestrogenicity in MCF-7 cells: modulation of hormone-induced cell cycle enzymes. Archives of Biochemistry and Biophysics, 356, 239-248.
128. Chen, I., Hsieh, T., Thomas, T., and Safe, S. (2001). Identification of estrogen-induced genes downregulated by AhR agonists in MCF-7 breast cancer cells using suppression subtractive hybridization. Gene, 262, 207-214.
129. Duan, R., Porter, W., Samudio, I., Vyhlidal, C., Kladde, M., and Safe, S. (1999). Transcriptional activation of c-fos protooncogene by 17beta-estradiol: mechanism of aryl hydrocarbon receptor-mediated inhibition. Molecular Endocrinology, 13, 1511-1521.
130. Wormke, M., Stoner, M., Saville, B., and Safe, S. (2000). Crosstalk between estrogen receptor alpha and the aryl hydrocarbon receptor in breast cancer cells involves unidirectional activation of proteasomes. FEBS Letters, 478, 109-112.
131. Wormke, M., Stoner, M., Saville, B.,Walker, K., Abdelrahim, M., Burghardt, R., and Safe, S. (2003). The aryl hydrocarbon receptor mediates degradation of estrogen receptor alpha through activation of proteasomes. Molecular and Cellular Biology, 23, 1843-1855.
132. Ohtake, F., Baba, A., Takada, I., Okada, M., Iwasaki, K., Miki, H., Takahashi, S., Kouzmenko, A., Nohara, K., Chiba, T., Fujii-Kuriyama, Y., and Kato, S. (2007). Dioxin receptor is a ligand-dependent E3 ubiquitin ligase. Nature, 446, 562-566.
133. Kociba, R. J.,Keyes, D. G., Beyer, J. E., Carreon, R. M.,Wade, C. E., Dittenber, D. A., Kalnins, R. P., Frauson, L. E., Park, C. N., Barnard, S. D., Hummel, R. A., and Humiston, C. G. (1978). Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicology and Applied Pharmacology, 46, 279-303.
134. Holcomb, M. and Safe, S. (1994). Inhibition of 7,12-dimethylbenzanthracene-induced rat mammary tumor growth by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Cancer Letters, 82, 43-47.
135. McDougal, A., Wilson, C., and Safe, S. (1997). Inhibition of 7,12-dimethyl-benz[a]anthracene-induced rat mammary tumor growth by aryl hydrocarbon receptor agonists. Cancer Letters, 120, 53-63.
136. Marquez-Bravo, L. G. and Gierthy, J. F. (2008). Differential expression of estrogen receptor alpha (ERalpha) protein in MCF-7 breast cancer cells chronically exposed to TCDD. Journal of Cellular Biochemistry, 103, 636-647.
137. Schlezinger, J. J., Liu, D., Farago, M., Seldin, D. C., Belguise, K., Sonenshein, G. E., and Sherr, D. H. (2006). A role for the aryl hydrocarbon receptor in mammary gland tumorigenesis. Biological Chemistry, 387, 1175-1187.
138. Dietrich, C. and Kaina, B. (2010). The aryl hydrocarbon receptor (AhR) in the regulation of cell-cell contact and tumor growth. Carcinogenesis, 31, 1319-1328.
139. Zhang, S., Lei, P., Liu, X., Li, X., Walker, K., Kotha, L., Rowlands, C., and Safe, S. (2009). The aryl hydrocarbon receptor as a target for estrogen receptor-negative breast cancer chemotherapy. Endocrine-Related Cancer, 16, 835-844.
140. Ma, Q. and Whitlock, J. P., Jr., (1996). The aromatic hydrocarbon receptor modulates Hepa1c1c7 cell cycle and differentiated state independently of dioxin. Molecular and Cellular Biology, 16, 2144-2150.
141. Elizondo, G., Fernandez-Salguero, P., Sheikh, M. S., Kim, G. Y., Fornace, A. J., Lee, K. S., and Gonzalez, F. J. (2000). Altered cell cycle control at the G(2)/M phases in aryl hydrocarbon receptor-null embryo fibroblast. Molecular Pharmacology, 57, 1056-1063.
142. Tohkin, M., Fukuhara, M., Elizondo, G., Tomita, S., and Gonzalez, F. J. (2000). Aryl hydrocarbon receptor is required for p300-mediated induction of DNA synthesis by adenovirus E1A. Molecular Pharmacology, 58, 845-851.
143. Chang, X., Fan,Y., Karyala, S., Schwemberger, S., Tomlinson, C. R., Sartor,M. A., and Puga, A. (2007). Ligand-independent regulation of transforming growth factor beta1 expression and cell cycle progression by the aryl hydrocarbon receptor. Molecular and Cellular Biology, 27, 6127-6139.
144. Zaher, H., Fernandez-Salguero, P. M., Letterio, J., Sheikh, M. S., Fornace, A. J., Jr., Roberts, A. B., and Gonzalez, F. J. (1998). The involvement of aryl hydrocarbon receptor in the activation of transforming growth factor-beta and apoptosis. Molecular Pharmacology, 54, 313-321.
145. Haarmann-Stemmann, T., Bothe, H., and Abel, J. (2009). Growth factors, cytokines and their receptors as downstream targets of aryl hydrocarbon receptor (AhR) signaling pathways. Biochemical Pharmacology, 77, 508-520.
146. Barhoover, M. A., Hall, J. M., Greenlee, W. F., and Thomas, R. S. (2010). Aryl hydrocarbon receptor regulates cell cycle progression in human breast cancer cells via a functional interaction with cyclin-dependent kinase 4. Molecular Pharmacology, 77, 195-201.
147. Döhr, O. and Abel, J. (1997). Transforming growth factorbeta1 coregulates mRNA expression of aryl hydrocarbon receptor and cell-cycle-regulating genes in human cancer cell lines. Biochemical and Biophysical Research Communications, 241, 86-91.
148. Levine-Fridman, A., Chen, L., and Elferink, C. (2004). Cytochrome P4501A1 promotes G1 phase cell cycle progression by controlling aryl hydrocarbon receptor activity. Molecular Pharmacology, 65, 461-4698.
149. Oesch-Bartlomowicz, B., Huelster, A., Wiss, O., Antoniou-Lipfert, P., Dietrich, C., Arand, M., Weiss, C., Bockamp, E., and Oesch, F. (2005). Aryl hydrocarbon receptor activation by cAMP vs. dioxin: divergent signaling pathways. Proceedings of the National Academy of Sciences of the United States of America, 102, 9218-9223.
150. 2+-mediated endonuclease activation. Science, 242, 256-259.
151. Kamath, A. B., Xu, H., Nagarkatti, P. S., and Nagarkatti, M. (1997). Evidence for the induction of apoptosis in thymocytes by 2,3,7,8-tetrachlorodibenzo-p-dioxin in vivo. Toxicology and Applied Pharmacology, 142, 367-377.
152. Pryputniewicz, S. J., Nagarkatti, M., and Nagarkatti, P. S. (1998). Differential induction of apoptosis in activated and resting T cells by 2,3,7,8-tetrachlorodibenzo-dioxin (TCDD) and its repercussion on T cell responsiveness. Toxicology, 129, 211-226.
153. Camacho, I. A., Hassuneh, M. R., Nagarkatti, M., and Nagarkatti, P. S. (2001). Enhanced activation-induced cell death as a mechanism of 2,3,7,8-tetrachlorodibenzo-dioxin (TCDD)-induced immunotoxicity in peripheral T cells. Toxicology, 165, 51-63.
154. Camacho, I. A., Nagarkatti, M., and Nagarkatti, P. S. (2002). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces Fas-dependent activation-induced cell death in superantigenprimed T cells. Archives of Toxicology, 76, 570-580.
155. Singh, N. P., Nagarkatti, M., and Nagarkatti, P. (2008). Primary peripheral T cells become susceptible to 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated apoptosis in vitro upon activation and in the presence of dendritic cells. Molecular Pharmacology, 73, 1722-1735.
156. Azkargorta, M., Fullaondo, A., Laresgoiti, U., Aloria, K., Infante, A., Arizmendi, J. M., and Zubiaga, A. M. (2010). Differential proteomics analysis reveals a role for E2F2 in the regulation of the AhR pathway in T lymphocytes. Molecular & Cellular Proteomics, 9, 2184-2194.
157. Sanchez-Martin, F. J., Fernandez-Salguero, P. M., and Merino, J. M. (2010). 2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptosis in neural growth factor (NGF)-differentiated pheochromocytoma PC12 cells. Neurotoxicology, 31, 267-276.
158. Savill, J., Fadok, V., Henson, P., and Haslett, C. (1993). Phagocyte recognition of cells undergoing apoptosis. Immunology Today, 14, 131-136.
159. Silverstone, A. E., Frazier, D. E., Jr. Fiore, N. C., Soults, J. A., and Gasiewicz, T. A. (1994). Dexamethasone, beta-estradiol, and 2,3,7,8-tetrachlorodibenzo-p-dioxin elicit thymic atrophy through different cellular targets. Toxicology and Applied Pharmacology, 126, 248-259.
160. 4+ T cells: the roles of apoptosis, Fas, and TNF. Toxicology, 170, 139-151.
161. Besteman, E. G., Zimmerman, K. L., and Holladay, S. D. (2005). Tetrachlorodibenzo-p-dioxin (TCDD) inhibits differentiation and increases apoptotic cell death of precursor T-cells in the fetal mouse thymus. Journal of Immunotoxicology, 2, 107-114.
162. Rhile, M. J., Nagarkatti, M., and Nagarkatti, P. S. (1996). Role of Fas apoptosis and MHC genes in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced immunotoxicity of T cells. Toxicology, 110, 153-167.
163. Krammer, P. H. (2000). CD95's deadly mission in the immune system. Nature, 407, 789-795.
164. Kamath, A. B., Camacho, I., Nagarkatti, P. S., and Nagarkatti, M. (1999). Role of Fas-Fas ligand interactions in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced immunotoxicity: increased resistance of thymocytes from Fas-deficient (lpr) and Fas ligand-defective (gld) mice to TCDD-induced toxicity. Toxicology andAppliedPharmacology, 160, 141-155.
165. Funatake, C. J., Dearstyne, E. A., Steppan, L. B., Shepherd, D. M., Spanjaard, E. S., Marshak-Rothstein, A., andKerkvliet, N. (2004). Early consequences of 2,3,7,8-tetrachlorodibenzop-dioxin exposure on the activation and survival of antigenspecific T cells. Toxicological Sciences, 82, 129-142.
166. Yoshizawa, K., Marsh, T., Foley, J. F., Cai, B., Peddada, S., Walker, N. J., and Nyska, A. (2005). Mechanisms of exocrine pancreatic toxicity induced by oral treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin in female Harlan Sprague-Dawley Rats. Toxicological Sciences, 85, 594-606.
167. Fisher, M. T., Nagarkatti, M., and Nagarkatti, P. S. (2003). Combined screening of thymocytes using apoptosis-specific cDNA array and promoter analysis yields novel gene targets mediating TCDD-induced toxicity. Toxicological Sciences, 78, 116-124.
168. Camacho, I. A., Singh, N., Hegde, V. L., Nagarkatti, M., and Nagarkatti, P. S. (2005). Treatment of mice with 2,3,7,8-tetrachlorodibenzo-p-dioxin leads to aryl hydrocarbon receptor-dependent nuclear translocation of NF-kappaB and expression of Fas ligand in thymic stromal cells and consequent apoptosis in T cells. Journal of Immunology, 175, 90-103.
169. Staples, J. E., Fiore, N. C., Frazier, D. E., Jr. Gasiewicz, T. A., and Silverstone, A. E. (1998). Overexpression of the antiapoptotic oncogene, bcl-2, in the thymus does not prevent thymic atrophy induced by estradiol or 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicology and Applied Pharmacology, 151, 200-210.
170. Wörner, W. and Schrenk, D. (1996). Influence of liver tumor promoters on apoptosis in rat hepatocytes induced by 2-acetylaminofluorene, ultraviolet light, or transforming growth factor beta 1. Cancer Research, 56, 1272-1278.
171. Wörner, W. and Schrenk, D. (1998). 2,3,7,8-Tetrachlorodibenzo-p-dioxin suppresses apoptosis and leads to hyperphosphorylation of p53 in rat hepatocytes. Environmental Toxicology and Pharmacology, 6, 239-247.
172. Chopra, M., Dharmarajan, A. M., Meiss, G., and Schrenk, D. (2009). Inhibition of UV-C light-induced apoptosis in liver cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicological Sciences, 111, 49-63.
173. Chopra, M., Gährs, M., Haben, M., Michels, C., and Schrenk, D. (2010). Inhibition of apoptosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin depends on protein biosynthesis. Cell Biology and Toxicology, 26, 391-401.
174. Christensen, J. G., Gonzales, A. J., Cattley, R. C., and Goldsworthy, T. L. (1998). Regulation of apoptosis in mouse hepatocytes and alteration of apoptosis by nongenotoxic carcinogens. Cell Growth & Differentiation, 9, 815-825.
175. Reiners, J. J., Jr. and Clift, R. E. (1999). Aryl hydrocarbon receptor regulation of ceramide-induced apoptosis in murine hepatoma 1c1c7 cells. A function independent of aryl hydrocarbon receptor nuclear translocator. Journal of Biological Chemistry, 274, 3505-2510.
176. Davis, J. W., II, Melendez, K., Salas, V. M., Lauer, F. T., and Burchiel, S. W. (2000). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibits growth factor withdrawal-induced apoptosis in the human mammary epithelial cell line, MCF-10A. Carcinogenesis, 21, 881-886.
177. Davis, J.W., II, Lauer, F. T., Burdick, A. D., Hudson, L. G., and Burchiel, S. W. (2001). Prevention of apoptosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the MCF-10A cell line: correlation with increased transforming growth factor a production. Cancer Research, 61, 3314-3320.
178. Davis, J. W., Jr. Burdick, A. D., Lauer, F. T., and Burchiel, S. W. (2003). The aryl hydrocarbon receptor antagonist, 3'-methoxy-4'-nitroflavone, attenuates 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent regulation of growth factor signaling and apoptosis in the MCF-10A cell line. Toxicology and Applied Pharmacology, 188, 42-49.
179. Park, S. and Matsumura, F. (2006). Characterization of antiapoptotic action of TCDD as a defensive cellular stress response reaction against the cell damaging action of ultraviolet irradiation in an immortalized normal human mammary epithelial cell line, MCF10A. Toxicology, 217, 139-146.
180. Vogel, C. F. A., Li,W., Sciullo, E., Newman, J., Hammock, B., Reader, J. R., Tuscano, J., and Matsumura, F. (2007). Pathogenesis of aryl hydrocarbon receptor-mediated development of lymphoma is associated with increased cyclooxygenase-2 expression. American Journal of Pathology, 171, 1538-1548.
181. Schrenk, D., Müller, M., Merlino, G., and Thorgeirsson, S. S. (1997). Interactions of TCDD with signal transduction and neoplastic development in c-myc transgenic and TGF-alpha transgenic mice. Archives of Toxicology Supplement, 19, 367-375.
182. Pääjärvi, G., Viluksela, M., Pohjanvirta, R., Stenius, U., and Högberg, J. (2005). TCDD activates Mdm2 and attenuates the p53 response to DNA damaging agents. Carcinogenesis, 26, 201-208.
183. Reyes-Hernández, O. D., Mejía-García, A., Sánchez-Ocampo, E. M., Cabañas-Cortés, M. A., Ramírez, P., Chávez-González, L., Gonzalez, F. J., and Elizondo, G. (2010). Ube2l3 gene expression is modulated by activation of the aryl hydrocarbon receptor: implications for p53 ubiquitination. Biochemical Pharmacology, 80, 932-940.
184. Llovet, J.M. and Bruix, J. (2008).Molecular targeted therapies in hepatocellular carcinoma. Hepatology, 48, 1312-1327.
185. Ambolet-Camoit, A., Bui, L. C., Pierre, S., Chevallier, A., Marchand, A., Coumoul, X., Garlatti, M., Andreau, K., Barouki, R., and Aggerbeck, M. (2010). 2,3,7,8-Tetrachlorodibenzo-p-dioxin counteracts the p53 response to a genotoxicant by upregulating expression of the metastasis marker agr2 in the hepatocarcinoma cell line HepG2. Toxicological Sciences, 115, 501-512.
186. Sarioglu, H., Brandner, S., Haberger, M., Jacobsen, C., Lichtmannegger, J., Wormke, M., and Andrae, U. (2008). Analysis of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced proteome changes in 5L rat hepatoma cells reveals novel targets of dioxin action including the mitochondrial apoptosis regulator VDAC2. Molecular & Cellular Proteomics, 7, 394-410.
187. Fernandez-Salguero, P., Pineau, T., Hilbert, D. M., McPhail, T., Lee, S. S., Kimura, S., Nebert, D. W., Rudikoff, S., Ward, J. M., and Gonzalez, F. J. (1995). Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor. Science, 268, 722-726.
188. Corchero, J., Martín-Partido, G., Dallas, S. L., and Fernández-Salguero, P. M. (2004). Liver portal fibrosis in dioxin receptor-null mice that overexpress the latent transforming growth factor-beta-binding protein-1. International Journal of Experimental Pathology, 85, 295-302.
189. Wu, R., Zhang, L., Hoagland, M. S., and Swanson, H. I. (2007). Lack of the aryl hydrocarbon receptor leads to impaired activation of AKT/protein kinase B and enhanced sensitivity to apoptosis induced via the intrinsic pathway. Journal of Pharmacology and Experimental Therapeutics, 320, 448-457.
190. Marlowe, J. L., Fan, Y., Chang, X., Peng, L., Knudsen, E. S., Xia, Y., and Puga, A. (2008). The aryl hydrocarbon receptor binds to E2F1 and inhibits E2F1-induced apoptosis. Molecular Biology of the Cell, 19, 3263-3271.
191. Tada, S. (2007). Cdt1 and geminin: role during cell cycle progression and DNA damage in higher eukaryotes. Frontiers in Bioscience, 12, 1629-1641.
192. Min/+ mice with natural ligands. Proceedings of the National Academy of Sciences of the United States of America, 106, 13481-13486.
193. Caruso, J. A., Mathieu, P. A., Joiakim, A., Zhang, H., and Reiners, J. J. Jr. (2006). Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent. Journal of Biological Chemistry, 281, 10954-10967.
194. Park, K. T., Mitchell, K. A., Huang, G., and Elferink, C. J. (2005). The aryl hydrocarbon receptor predisposes hepatocytes to Fas-mediated apoptosis. Molecular Pharmacology, 67, 612-622.
195. Majora, M., Frericks, M., Temchura, V., Reichmann, G., and Esser, C. (2005). Detection of a novel population of fetal thymocytes characterized by preferential emigration and a TCRgammadelta + T cell fate after dioxin exposure. International Immunopharmacology, 5, 1659-1674.
196. Safe, S. and Wormke, M. (2003). Inhibitory aryl hydrocarbon receptor-estrogen receptor alpha cross-talk and mechanisms of action. Chemical Research in Toxicology, 16, 807-816.
197. Warner, M., Eskenazi, B., Mocarelli, P., Gerthoux, P. M., Samuels, S., Needham, L., Patterson, D., and Brambilla, P. (2002). Serum dioxin concentrations and breast cancer risk in the Seveso Women's Health Study. Environmental Health Perspectives, 110, 625-628.
198. Pesatori, A. C., Consonni, D., Rubagotti, M., Grillo, P., and Bertazzi, P. A. (2009). Cancer incidence in the population exposed to dioxin after the "Seveso accident": twenty years of follow-up. Environmental Health, 8, 39.