Induction of p21(waf1) expression and growth inhibition by transforming growth factor β involve the tumor suppressor gene DPC4 in human pancreatic adenocarcinoma cells

Cancer Research

Volumn 57, Issue 18, 1997, Pages 3929-3934

  Grau, Ana M ^a,b   Zhang, Ling ^a   Wang, Weixin ^a   Ruan, Sanbao ^a   Evans, Douglas B ^a   Abbruzzese, James L ^a   Zhang, Wei ^a   Chiao, Paul J ^a  

^a UNIVERSITY OF TEXAS   (United States)

^b UNIVERSITY OF ARIZONA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P21; TRANSFORMING GROWTH FACTOR BETA RECEPTOR; CDKN1A PROTEIN, HUMAN; CYCLIN DEPENDENT KINASE INHIBITOR 1A; CYCLINE; DNA BINDING PROTEIN; MESSENGER RNA; RNA; SMAD4 PROTEIN; SMAD4 PROTEIN, HUMAN; TRANSACTIVATOR PROTEIN; TRANSFORMING GROWTH FACTOR BETA;

ARTICLE; CARCINOMA CELL; CELL PROLIFERATION; GENE INDUCTION; GROWTH INHIBITION; HUMAN; HUMAN CELL; IRRADIATION; PANCREAS ADENOCARCINOMA; PRIORITY JOURNAL; PROMOTER REGION; REPORTER GENE; SIGNAL TRANSDUCTION; TRANSCRIPTION REGULATION; TUMOR GROWTH; TUMOR SUPPRESSOR GENE; ADENOCARCINOMA; CELL CULTURE; CELL DIVISION; GENE EXPRESSION REGULATION; GENETICS; PANCREAS TUMOR; PATHOLOGY; PHYSIOLOGY;

ADENOCARCINOMA; CELL DIVISION; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; DNA-BINDING PROTEINS; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, TUMOR SUPPRESSOR; HUMANS; PANCREATIC NEOPLASMS; RNA, MESSENGER; RNA, NEOPLASM; SMAD4 PROTEIN; TRANS-ACTIVATORS; TRANSFORMING GROWTH FACTOR BETA; TUMOR CELLS, CULTURED;

EID: 0030612484     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (26)

1. Parker, S. L., Tong, T., Bolden, S., and Wingo, P. A. Cancer statistics, 1997. CA Cancer J. Clin., 47: 5-27, 1997.
2. DiGiuseppe, J. A., Yeo, C. J., and Hruban, R. H. Molecular biology and the diagnosis and treatment of adenocarcinoma of the pancreas. Adv. Anat. Pathol., 3: 139-155,
3. Staley, C. A., Lee, J. E., Cleary, K. A., Abbruzzese, J. L., Ames, F. C., Fenoglio, C., and Evans, D. B. Preoperative chemoradiation, pancreaticoduodenectomy, and intraoperative radiation therapy for adenocarcinoma of the pancreatic head: patient survival and patterns of treatment failure. Am. J. Surg., 171: 118-124, 1996.
4. Evans, D. B., Abbruzzese, J. L., Lee, J. E., Leach, S. D., Charnsangavej, C., Cleary, K. R., Buchholz, D. J., and Rich, T. A. Preoperative chemoradiation for adenocarcinoma of the pancreas: M. D. Anderson experience. Semin. Surg. Oncol., 11: 132-142, 1995.
5. Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., DaCosta, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., and Kern, S. E. DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. Science (Washington DC), 271: 350-353, 1996.
6. Hoodless, P. A., Haerry, T., Abdollah, S., Stapleton, M., O'Connor, M. B., Attisano, L., and Wrana, J. L. MADR1, a mad-related protein that functions in BMP2 signaling pathways. Cell, 85: 489-500, 1996.
7. Graff, J. M., Bansal, A., and Melton, D. A. Xenopus mad proteins transduce distinct subsets of signals for the TGF-β superfamily. Cell, 85: 479-487, 1996.
8. Zhang, Y., Feng, X. H., Wu, R. Y., and Derynck, R. Receptor-associated Mad homologues synergize as effectors of the TGF-β response. Nature (Lond.), 383: 168-172, 1996.
9. Massague, J. TGF-β signaling: receptors, transducers, and mad proteins. Cell, 85: 947-950, 1996.
10. Fynan, T. M., and Reiss, M. Resistance to inhibition of cell growth by transforming growth factor β and its role in oncogenesis. Crit. Rev. Oncog., 4: 493-540, 1993.
11. Kretzschmar, M., Liu, F., Hata, A., Doody, J., and Massague, J. The TGF-β family mediator Smad1 is phosphorylated directly and activated functionally by the BMP receptor kinase. Genes Dev., 11: 984-995, 1997.
12. Lagna, G., Hata, A., Hemmati-Brivanlou, A., and Massague, J. Partnership between DPC4 and SMAD proteins in TGF-β signalling pathways. Nature (Lond.), 383: 832-836, 1996.
13. Datto, M. B., Yu, Y., and Wang, X. F. Functional analysis of the transforming growth factor β responsive elements in the WAF1/CIP1/p21 promoter. J. Biol. Chem., 270: 28623-28628, 1995.
14. waf1 induction are important early events. Cell Growth Differ., 7: 1291-1304, 1996.
15. Baldwin, R. L., and Korc, M. Growth inhibition of human pancreatic carcinoma cells by transforming growth factor β1. Growth Factors, 8: 23-34, 1993.
16. Sambrook, J., Fritsch, E. F., and Maniatis, T. Protocol I. In: C. Nolan (ed.), Molecular Cloning: A Laboratory Manual, Vol. 2, pp. 9.16-9.19. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1989.
17. Chomczynski, P., and Sacchi, N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol chloroform extraction. Anal. Biochem., 162: 156-159, 1987.
18. Zhang, W., Grasso, L., McClain, C. D., Gamble, A. M., Cha, Y., Travali, S., Deisseroth, A. B., and Mercer, W. E. p53-independent induction of WAF1/Cip1 in human myeloid leukemia cells is correlated with growth arrest accompanying monocyte/macrophage differentiation. Cancer Res., 55: 668-674, 1995.
19. Freeman, J. W., Mattingly, C. A., and Strodel, W. E. Increased tumorigenicity in the human pancreatic cell line MIA PaCa-2 is associated with an aberrant regulation of an IGF-1 autocrine loop and lack of expression of the TGF-β type RII receptor. J. Cell. Physiol., 165: 155-163, 1995.
20. DiGiuseppe, J. A., Redston, M. S., Yeo, C. J., Kern, S. E., and Hruban, R. H. p53-independent expression of the cyclin-dependent kinase inhibitor p21 in pancreatic carcinoma. Am. J. Pathol., 147: 884-888, 1995.
21. Barton, C. M., Staddon, S. L., Hughes, C. M., Hall, P. A., O'Sullivan, C., Kloppel, G., Theis, B., Russell, R. C. G., Neoptolemos, J., Williamson, R. C. N., Lane, D. P., and Lemoine, N. R. Abnormalities of the p53 tumour suppressor gene in human pancreatic cancer. Br. J. Cancer, 64: 1076-1082, 1991.
22. Li, Y. J., Salmon, L-P. P., Thomas, G., and Hamelin, R. Polymorphisms and probable lack of mutation in the WAF1-CIP1 gene in colorectal cancer. Oncogene, 10: 599-601, 1995.
23. Xiong, Y., Hamnon, G. J., Zhang, H., Casso, D., Kobayaashi, R., and Beach, D. p21 is a universal inhibitor of cyclin kinases. Nature (Lond.), 366: 701-704, 1993.
24. Labaer, J., Garrett, M. D., Stevenson, L. F., Slingerland, J. M., Sandhu, C., Chou, H. S., Fattaey, A., and Harlow, E. New functional activities for the p21 family of CDK inhibitors. Genes Dev., 11: 847-862, 1997.
25. Perkins, N. D., Felzien, L. K., Betts, J. C., Leung, K., Beach, D. H., and Nabel, G. J. Regulation of NF-κB by cyclin-dependent kinases associated with the p300 coactivator. Science (Washington DC), 275: 523-527, 1997.
26. Baldwin, R. L., Friess, H., Yokoyama, M., Lopez, M., Kobrin, M. S., Buchler, M. W., and Korc, M. Attenuated ALK5 receptor expression in human pancreatic cancer: correlation with resistance to growth inhibition. Int. J. Cancer, 67: 283-288, 1996.