Epithelial-mesenchymal-transition regulators in prostate cancer: Androgens and beyond

Journal of Steroid Biochemistry and Molecular Biology

Volumn 166, Issue , 2017, Pages 84-90

  Nakazawa, Mary ^a   Kyprianou, Natasha ^a  

^a UNIVERSITY OF KENTUCKY   (United States)

Author keywords

Androgen receptor; Cell plasticity; Epithelial transitions; Metastasis; Prostate cancer; Resistance; Therapeutic

Indexed keywords

ANDROGEN; ANTINEOPLASTIC AGENT; NOTCH RECEPTOR; PROTEIN TYROSINE KINASE; SONIC HEDGEHOG PROTEIN; TRANSFORMING GROWTH FACTOR BETA; ANDROGEN RECEPTOR; AR PROTEIN, HUMAN; LIGAND; TAXOID; TRANSCRIPTION FACTOR; TUMOR MARKER; WNT PROTEIN;

CANCER GROWTH; CANCER PATIENT; CANCER RESISTANCE; CANCER THERAPY; EPITHELIAL MESENCHYMAL TRANSITION; HUMAN; MALE; PHENOTYPE; PROSTATE CANCER; REVIEW; SIGNAL TRANSDUCTION; TRANSCRIPTION REGULATION; TUMOR MICROENVIRONMENT; ANIMAL; CHEMISTRY; DRUG RESISTANCE; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; METASTASIS; MOUSE; PROSTATIC NEOPLASMS; PROSTATIC NEOPLASMS, CASTRATION-RESISTANT;

ANDROGENS; ANIMALS; ANTINEOPLASTIC AGENTS; BIOMARKERS, TUMOR; DRUG RESISTANCE, NEOPLASM; EPITHELIAL-MESENCHYMAL TRANSITION; GENE EXPRESSION REGULATION, NEOPLASTIC; HEDGEHOG PROTEINS; HUMANS; LIGANDS; MALE; MICE; NEOPLASM METASTASIS; PHENOTYPE; PROSTATIC NEOPLASMS; PROSTATIC NEOPLASMS, CASTRATION-RESISTANT; RECEPTORS, ANDROGEN; RECEPTORS, NOTCH; SIGNAL TRANSDUCTION; TAXOIDS; TRANSCRIPTION FACTORS; WNT PROTEINS;

EID: 84973473567     PISSN: 09600760     EISSN: 18791220     Source Type: Journal    
DOI: 10.1016/j.jsbmb.2016.05.007     Document Type: Review

References (110)

1. [1] Siegel, R.L., Miller, K.D., Jemal, A., Cancer statistics 2015. CA. Cancer J. Clin. 65 (2015), 5–29.
2. [2] Klotz, L., Zhang, L., Lam, A., Nam, R., Mamedov, A., Loblaw, A., Clinical results of long-term follow-up of a large, active surveillance cohort with localized prostate cancer. J. Clin. Oncol. 28 (2010), 126–131.
3. [3] Crawford, E., Challenges in the management of prostate cancer. Br. J. Urol. 70 (1992), 33–38.
4. [4] Higano, C.S., Crawford, E.D., New and emerging agents for the treatment of castration-resistant prostate cancer. Urol. Oncol. 29 (2011), S1–8.
5. [5] Scher, H.I., Sawyers, C.L., Biology of progressive, castration-resistant prostate cancer: directed therapies targeting the androgen-receptor signaling axis. J. Clin. Oncol. 23 (2005), 8253–8261.
6. [6] Carlin, B.I., Andriole, G.L., The natural history, skeletal complications, and management of bone metastases in patients with prostate carcinoma. Cancer 88 (2000), 2989–2994.
7. [7] Logothetis, C.J., Lin, S.-H., Osteoblasts in prostate cancer metastasis to bone. Nat. Rev. Cancer 5 (2005), 21–28.
8. [8] Chung, L.W., Baseman, A., Assikis, V., Zhau, H.E., Molecular insights into prostate cancer progression: the missing link of tumor microenvironment. J. Urol. 173 (2005), 10–20.
9. [9] Yilmaz, M., Christofori, G., EMT, the cytoskeleton, and cancer cell invasion. Cancer Metastasis Rev. 28 (2009), 15–33.
10. [10] Thiery, J.P., Acloque, H., Huang, R.Y., Nieto, M.A., Epithelial-mesenchymal transitions in development and disease. Cell 139 (2009), 871–890.
11. [11] van der Pluijm, G., Epithelial plasticity, cancer stem cells and bone metastasis formation. Bone 48 (2011), 37–43.
12. [12] Ouyang, G., Wang, Z., Fang, X., Liu, J., Yang, C.J., Molecular signaling of the epithelial to mesenchymal transition in generating and maintaining cancer stem cells. Cell. Mol. life Sci. 67 (2010), 2605–2618.
13. [13] Brabletz, T., To differentiate or not – routes towards metastasis. Nat. Rev. Cancer 12 (2012), 425–436.
14. [14] de Bono, J.S., Logothetis, C.J., Molina, A., Fizazi, K., North, S., Chu, L., Chi, K.N., Jones, R.J., Goodman, O.B., Saad, F., Staffurth, J.N., Mainwaring, P., Harland, S., Flaig, T.W., Hutson, T.E., Cheng, T., Patterson, H., Hainsworth, J.D., Ryan, C.J., Sternberg, C.N., Ellard, S.L., Fléchon, A., Saleh, M., Scholz, M., Efstathiou, E., Zivi, A., Bianchini, D., Loriot, Y., Chieffo, N., Kheoh, T., Haqq, C.M., Scher, H.I., Abiraterone and increased survival in metastatic prostate cancer. New Engl. J. Med. 364 (2011), 1995–2005.
15. [15] Scher, H.I., Fizazi, K., Saad, F., Taplin, M.-E., Sternberg, C.N., Miller, K., de Wit, R., Mulders, P., Chi, K.N., Shore, N.D., Armstrong, A.J., Flaig, T.W., Fléchon, A., Mainwaring, P., Fleming, M., Hainsworth, J.D., Hirmand, M., Selby, B., Seely, L., de Bono, J.S., Increased survival with enzalutamide in prostate cancer after chemotherapy. New Engl. J. Med. 367 (2012), 1187–1197.
16. [16] Martin, S.K., Banuelos, C.A., Sadar, M.D., Kyprianou, N., N-terminal targeting of androgen receptor variant enhances response of castration resistant prostate cancer to taxane chemotherapy. Mol. Oncol. 9 (2015), 628–639.
17. [17] Martin, S.K., Pu, H., Penticuff, J.C., Cao, Z., Horbinski, C., Kyprianou, N., Multinucleation and mesenchymal-to-epithelial transition alleviate resistance to combined cabazitaxel and antiandrogen therapy in advanced prostate cancer. Cancer Res., 2015.
18. [18] Kalluri, R., The basics of epithelial-mesenchymal transition 119 (2009), 1420–1428.
19. [19] Cano, A., Perez-Moreno, M.A., Rodrigo, I., Locascio, A., Blanco, M.J., del Barrio, M.G., Portillo, F., Nieto, M.A., The transcription factor Snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression. Nat. Cell Biol. 2 (2000), 76–83.
20. [20] Batlle, E., Sancho, E., Franci, C., Dominguez, D., Monfar, M., Baulida, J., Garcia De Herreros, A., The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumour cells. Nat. Cell Biol. 2 (2000), 84–89.
21. [21] Thiery, J.P., Epithelial-mesenchymal transitions in tumour progression. Nat. Rev. Cancer 2 (2002), 442–454.
22. [22] Guarino, M., Rubino, B., Ballabio, G., The role of epithelial-mesenchymal transition in cancer pathology. Pathology (Phila.) 39 (2007), 305–318.
23. [23] Onder, T.T., Gupta, P.B., Mani, S.A., Yang, J., Lander, E.S., Weinberg, R.A., Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways. Cancer Res. 68 (2008), 3645–3654.
24. [24] Graff, J.R., Herman, J.G., Lapidus, R.G., Chopra, H., Xu, R., Jarrard, D.F., Isaacs, W.B., Pitha, P.M., Davidson, N.E., Baylin, S.B., E-cadherin expression is silenced by DNA hypermethylation in human breast and prostate carcinomas. Cancer Res. 55 (1995), 5195–5199.
25. [25] Davies, G., Jiang, W.G., Mason, M.D., Matrilysin mediates extracellular cleavage of E-cadherin from prostate cancer cells: a key mechanism in hepatocyte growth factor/scatter factor-induced cell–cell dissociation and in vitro invasion. Clin. Cancer Res. 7 (2001), 3289–3297.
26. [26] Umbas, R., Schalken, J.A., Aalders, T.W., Carter, B.S., Karthaus, H.F.M., Schaafsma, H.K., Debruyne, F.M.J., Isaacs, W.B., Expression of the cellular adhesion molecule E-cadherin is reduced or absent in high-grade prostate cancer. Cancer Res. 52 (1992), 5104–5109.
27. [27] Umbas, R., Isaacs, W.B., Bringuier, P.P., Schaafsma, H.E., Karthaus, H.F., Oosterhof, G.O., Debruyne, F.M., Schalken, J.A., Decreased E-cadherin expression is associated with poor prognosis in patients with prostate cancer. Cancer Res. 54 (1994), 3929–3933.
28. [28] Bergerheim, U.S., Kunimi, K., Collins, V.P., Ekman, P., Deletion mapping of chromosomes 8, 10, and 16 in human prostatic carcinoma. Genes Chromosomes Cancer 3 (1991), 215–220.
29. [29] Chu, K., Cheng, C.-J., Ye, X., Lee, Y.-C., Zurita, A.J., Chen, D.-T., Yu-Lee, L.-Y., Zhang, S., Yeh, E.T., Hu, M.C.-T., Logothetis, C.J., Lin, S.-H., Cadherin-11 promotes the metastasis of prostate cancer cells to bone. Mol. Cancer Res. 6 (2008), 1259–1267.
30. [30] Tran, N.L., Nagle, R.B., Cress, A.E., Heimark, R.L., N-cadherin expression in human prostate carcinoma cell lines. An epithelial-mesenchymal transformation mediating adhesion with Stromal cells. Am. J. Pathol. 155 (1999), 787–798.
31. [31] Bussemakers, M.J., Van Bokhoven, A., Tomita, K., Jansen, C.F., Schalken, J.A., Complex cadherin expression in human prostate cancer cells: international journal of cancer. J. Int. du Cancer 85 (2000), 446–450.
32. [32] Nieman, M.T., Prudoff, R.S., Johnson, K.R., Wheelock, M.J., N-cadherin promotes motility in human breast cancer cells regardless of their E-cadherin expression. J. Cell Biol. 147 (1999), 631–644.
33. [33] Jaggi, M., Nazemi, T., Abrahams, N.A., Baker, J.J., Galich, A., Smith, L.M., Balaji, K., N-cadherin switching occurs in high Gleason grade prostate cancer. Prostate 66 (2006), 193–199.
34. [34] Gravdal, K., Halvorsen, O.J., Haukaas, S.A., Akslen, L.A., A switch from E-cadherin to N-cadherin expression indicates epithelial to mesenchymal transition and is of strong and independent importance for the progress of prostate cancer. Clin. Cancer Res. 13 (2007), 7003–7011.
35. [35] Tanaka, H., Kono, E., Tran, C.P., Miyazaki, H., Yamashiro, J., Shimomura, T., Fazli, L., Wada, R., Huang, J., Vessella, R.L., An, J., Horvath, S., Gleave, M., Rettig, M.B., Wainberg, Z.A., Reiter, R.E., Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance. Nat. Med. 16 (2010), 1414–1420.
36. [36] Kallakury, B.V., Sheehan, C.E., Winn-Deen, E., Oliver, J., Fisher, H.A., Kaufman, R.P. Jr., Ross, J.S., Decreased expression of catenins (alpha and beta), p120CTN, and E-cadherin cell adhesion proteins and E-cadherin gene promoter methylation in prostatic adenocarcinomas. Cancer 92 (2001), 2786–2795.
37. [37] Satelli, A., Li, S., Vimentin as a potential molecular target in cancer therapy Or Vimentin, an overview and its potential as a molecular target for cancer therapy. Cell. Mol. Life Sci. 68 (2011), 3033–3046.
38. [38] Singh, S., Sadacharan, S., Su, S., Belldegrun, A., Persad, S., Singh, G., Overexpression of vimentin: role in the invasive phenotype in an androgen-independent model of prostate cancer. Cancer Res. 63 (2003), 2306–2311.
39. [39] Kolijn, K., Verhoef, E.I., van Leenders, G.J., Morphological and immunohistochemical identification of epithelial-to-mesenchymal transition in clinical prostate cancer. Oncotarget 6 (2015), 24488–24498.
40. [40] Bierie, B., Moses, H.L., Tumour microenvironment: TGF[beta]: the molecular Jekyll and Hyde of cancer. Nat. Rev. Cancer 6 (2006), 506–520.
41. [41] Massagué, J., TGFβ in cancer. Cell 134 (2008), 215–230.
42. [42] Micalizzi, D.S., Wang, C.-A., Farabaugh, S.M., Schiemann, W.P., Ford, H.L., Homeoprotein six1 increases TGF-β type I receptor and converts TGF-β signaling from suppressive to supportive for tumor growth. Cancer Res. 70 (2010), 10371–10380.
43. [43] Levy, L., Hill, C.S., Alterations in components of the TGF-β superfamily signaling pathways in human cancer. Cytokine Growth Factor Rev. 17 (2006), 41–58.
44. [44] Wikström, P., Stattin, P., Franck-Lissbrant, I., Damber, J.-E., Bergh, A., Transforming growth factor β1 is associated with angiogenesis, metastasis, and poor clinical outcome in prostate cancer. Prostate 37 (1998), 19–29.
45. [45] Kim, I.Y., Ahn, H.J., Lang, S., Oefelein, M.G., Oyasu, R., Kozlowski, J.M., Lee, C., Loss of expression of transforming growth factor-beta receptors is associated with poor prognosis in prostate cancer patients. Clin. Cancer Res. 4 (1998), 1625–1630.
46. [46] Lamouille, S., Xu, J., Derynck, R., Molecular mechanisms of epithelial-mesenchymal transition. Nat. Rev. Mol. Cell Biol. 15 (2014), 178–196.
47. [47] Zhang, Y.E., Non-smad pathways in TGF-[beta] signaling. Cell Res. 19 (2009), 128–139.
48. [48] Zavadil, J., Bitzer, M., Liang, D., Yang, Y.C., Massimi, A., Kneitz, S., Piek, E., Bottinger, E.P., Genetic programs of epithelial cell plasticity directed by transforming growth factor-beta. Proc. Natl. Acad. Sci. U.S.A. 98 (2001), 6686–6691.
49. [49] Bakin, A.V., Tomlinson, A.K., Bhowmick, N.A., Moses, H.L., Arteaga, C.L., Phosphatidylinositol 3-kinase function is required for transforming growth factor beta-mediated epithelial to mesenchymal transition and cell migration. J. Biol. Chem. 275 (2000), 36803–36810.
50. [50] Nagaraj, N.S., Datta, P.K., Targeting the transforming growth factor-β signaling pathway in human cancer. Expert Opin. Investig. Drugs 19 (2010), 77–91.
51. [51] Itoh, S., Thorikay, M., Kowanetz, M., Moustakas, A., Itoh, F., Heldin, C.H., ten Dijke, P., Elucidation of Smad requirement in transforming growth factor-beta type I receptor-induced responses. J. Biol. Chem. 278 (2003), 3751–3761.
52. [52] Chaudhury, A., The Tale of Transforming Growth Factor-β (TGFβ) Signaling. A Soigné Enigma 61 (2009), 929–939.
53. [53] Mak, P., Leav, I., Pursell, B., Bae, D., Yang, X., Taglienti, C.A., Gouvin, L.M., Sharma, V.M., Mercurio, A.M., ERβ impedes prostate cancer EMT by destabilizing HIF-1α and inhibiting VEGF-Mediated snail nuclear localization: implications for gleason grading. Cancer Cell 17 (2010), 319–332.
54. [54] Zhu, B., Fukada, K., Zhu, H., Kyprianou, N., Prohibitin and cofilin are intracellular effectors of transforming growth factor β signaling in human prostate cancer cells. Cancer Res. 66 (2006), 8640–8647.
55. [55] Collazo, J., Zhu, B., Larkin, S., Martin, S.K., Pu, H., Horbinski, C., Koochekpour, S., Kyprianou, N., Cofilin drives cell-invasive and metastatic responses to TGF-beta in prostate cancer. Cancer Res. 74 (2014), 2362–2373.
56. [56] Zhu, M.L., Partin, J.V., Bruckheimer, E.M., Strup, S.E., Kyprianou, N., TGF-beta signaling and androgen receptor status determine apoptotic cross-talk in human prostate cancer cells. Prostate 68 (2008), 287–295.
57. [57] Grunert, S., Jechlinger, M., Beug, H., Diverse cellular and molecular mechanisms contribute to epithelial plasticity and metastasis. Nat. Rev. Mol. Cell Biol. 4 (2003), 657–665.
58. [58] Gan, Y., Shi, C., Inge, L., Hibner, M., Balducci, J., Huang, Y., Differential roles of ERK and Akt pathways in regulation of EGFR-mediated signaling and motility in prostate cancer cells. Oncogene 29 (2010), 4947–4958.
59. [59] Kong, D., Wang, Z., Sarkar, S.H., Li, Y., Banerjee, S., Saliganan, A., Kim, H.R., Cher, M.L., Sarkar, F.H., Platelet-derived growth factor-D overexpression contributes to epithelial-mesenchymal transition of PC3 prostate cancer cells. Stem Cells 26 (2008), 1425–1435.
60. [60] Taylor, B.S., Schultz, N., Hieronymus, H., Gopalan, A., Xiao, Y., Carver, B.S., Arora, V.K., Kaushik, P., Cerami, E., Reva, B., Antipin, Y., Mitsiades, N., Landers, T., Dolgalev, I., Major, J.E., Wilson, M., Socci, N.D., Lash, A.E., Heguy, A., Eastham, J.A., Scher, H.I., Reuter, V.E., Scardino, P.T., Sander, C., Sawyers, C.L., Gerald, W.L., Integrative genomic profiling of human prostate cancer. Cancer Cell 18 (2010), 11–22.
61. [61] Mulholland, D.J., Kobayashi, N., Ruscetti, M., Zhi, A., Tran, L.M., Huang, J., Gleave, M., Wu, H., Pten loss and RAS/MAPK activation cooperate to promote EMT and metastasis initiated from prostate cancer stem/progenitor cells. Cancer Res. 72 (2012), 1878–1889.
62. [62] Zhou, B.P., Deng, J., Xia, W., Xu, J., Li, Y.M., Gunduz, M., Hung, M.C., Dual regulation of Snail by GSK-3beta-mediated phosphorylation in control of epithelial-mesenchymal transition. Nat. Cell Biol. 6 (2004), 931–940.
63. [63] Truica, C.I., Byers, S., Gelmann, E.P., Beta-catenin affects androgen receptor transcriptional activity and ligand specificity. Cancer Res. 60 (2000), 4709–4713.
64. [64] Fan, L., Pepicelli, C.V., Dibble, C.C., Catbagan, W., Zarycki, J.L., Laciak, R., Gipp, J., Shaw, A., Lamm, M.L., Munoz, A., Lipinski, R., Thrasher, J.B., Bushman, W., Hedgehog signaling promotes prostate xenograft tumor growth. Endocrinology 145 (2004), 3961–3970.
65. [65] Karhadkar, S.S., Steven Bova, G., Abdallah, N., Dhara, S., Gardner, D., Maitra, A., Isaacs, J.T., Berman, D.M., Beachy, P.A., Hedgehog signalling in prostate regeneration, neoplasia and metastasis. Nature 431 (2004), 707–712.
66. [66] Li, X., Deng, W., Nail, C.D., Bailey, S.K., Kraus, M.H., Ruppert, J.M., Lobo-Ruppert, S.M., Snail induction is an early response to Gli1 that determines the efficiency of epithelial transformation. Oncogene 25 (2006), 609–621.
67. [67] Peinado, H., Olmeda, D., Cano, A., Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?. Nat. Rev. Cancer 7 (2007), 415–428.
68. [68] Yang, M.H., Wu, M.Z., Chiou, S.H., Chen, P.M., Chang, S.Y., Liu, C.J., Teng, S.C., Wu, K.J., Direct regulation of TWIST by HIF-1alpha promotes metastasis. Nat. Cell Biol. 10 (2008), 295–305.
69. [69] Lu, X., Kang, Y., Hypoxia and hypoxia-Inducible factors: master regulators of metastasis. Clin. Cancer Res. 16 (2010), 5928–5935.
70. [70] Xu, J., Lamouille, S., Derynck, R., TGF-[beta]-induced epithelial to mesenchymal transition. Cell Res. 19 (2009), 156–172.
71. [71] Dave, N., Guaita-Esteruelas, S., Gutarra, S., Frias, A., Beltran, M., Peiro, S., de Herreros, A.G., Functional cooperation between Snail1 and twist in the regulation of ZEB1 expression during epithelial to mesenchymal transition. J. Biol. Chem. 286 (2011), 12024–12032.
72. [72] Hemavathy, K., Ashraf, S.I., Ip, Y.T., Snail/slug family of repressors: slowly going into the fast lane of development and cancer. Gene 257 (2000), 1–12.
73. [73] Cho, H.J., Baek, K.E., Saika, S., Jeong, M.-J., Yoo, J., Snail is required for transforming growth factor-β-induced epithelial–mesenchymal transition by activating PI3 kinase/Akt signal pathway. Biochem. Biophys. Res. Commun. 353 (2007), 337–343.
74. [74] Heeboll, S., Borre, M., Ottosen, P.D., Dyrskjot, L., Orntoft, T.F., Torring, N., Snail1 is over-expressed in prostate cancer, APMIS: acta pathologica, microbiologica. et immunologica Scandinavica 117 (2009), 196–204.
75. [75] Liu, Y.N., Abou-Kheir, W., Yin, J.J., Fang, L., Hynes, P., Casey, O., Hu, D., Wan, Y., Seng, V., Sheppard-Tillman, H., Martin, P., Kelly, K., Critical and reciprocal regulation of KLF4 and SLUG in transforming growth factor beta-initiated prostate cancer epithelial-mesenchymal transition. Mol. Cell. Biol. 32 (2012), 941–953.
76. [76] Zheng, H., Kang, Y., Multilayer control of the EMT master regulators. Oncogene 33 (2014), 1755–1763.
77. [77] Postigo, A.A., Depp, J.L., Taylor, J.J., Kroll, K.L., Regulation of Smad signaling through a differential recruitment of coactivators and corepressors by ZEB proteins. EMBO J. 22 (2003), 2453–2462.
78. [78] Byles, V., Zhu, L., Lovaas, J.D., Chmilewski, L.K., Wang, J., Faller, D.V., Dai, Y., SIRT1 induces EMT by cooperating with EMT transcription factors and enhances prostate cancer cell migration and metastasis. Oncogene 31 (2012), 4619–4629.
79. [79] Graham, T.R., Zhau, H.E., Odero-Marah, V.A., Osunkoya, A.O., Kimbro, K.S., Tighiouart, M., Liu, T., Simons, J.W., O'Regan, R.M., Insulin-like growth factor-I–dependent up-regulation of ZEB1 drives epithelial-to-mesenchymal transition in human prostate cancer cells. Cancer Res. 68 (2008), 2479–2488.
80. [80] Puisieux, A., Valsesia-Wittmann, S., Ansieau, S., A twist for survival and cancer progression. Br. J. Cancer 94 (2005), 13–17.
81. [81] Ansieau, S., Bastid, J., Doreau, A., Morel, A.-P., Bouchet, B.P., Thomas, C., Fauvet, F., Puisieux, I., Doglioni, C., Piccinin, S., Maestro, R., Voeltzel, T., Selmi, A., Valsesia-Wittmann, S., Caron de Fromentel, C., Puisieux, A., Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence. Cancer Cell 14 (2008), 79–89.
82. [82] Yuen, H.F., Chua, C.W., Chan, Y.P., Wong, Y.C., Wang, X., Chan, K.W., Significance of TWIST and E-cadherin expression in the metastatic progression of prostatic cancer. Histopathology 50 (2007), 648–658.
83. [83] Kwok, W.K., Ling, M.-T., Lee, T.-W., Lau, T.C.M., Zhou, C., Zhang, X., Chua, C.W., Chan, K.W., Chan, F.L., Glackin, C., Wong, Y.-C., Wang, X., Up-regulation of TWIST in prostate cancer and its implication as a therapeutic target. Cancer Res. 65 (2005), 5153–5162.
84. [84] Huggins, C., Stevens, R.E. Jr, Hodges, C.V., Studies on prostatic cancer: ii. the effects of castration on advanced carcinoma of the prostate gland. Arch. Surg. 43 (1941), 209–223.
85. [85] Koivisto, P., Kononen, J., Palmberg, C., Tammela, T., Hyytinen, E., Isola, J., Trapman, J., Cleutjens, K., Noordzij, A., Visakorpi, T., Kallioniemi, O.P., Androgen receptor gene amplification: a possible molecular mechanism for androgen deprivation therapy failure in prostate cancer. Cancer Res. 57 (1997), 314–319.
86. [86] Visakorpi, T., Hyytinen, E., Koivisto, P., Tanner, M., Keinanen, R., Palmberg, C., Palotie, A., Tammela, T., Isola, J., Kallioniemi, O.P., In vivo amplification of the androgen receptor gene and progression of human prostate cancer. Nat. Genet. 9 (1995), 401–406.
87. [87] Chang, K.H., Li, R., Papari-Zareei, M., Watumull, L., Zhao, Y.D., Auchus, R.J., Sharifi, N., Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer. Proc. Natl. Acad. Sci. U.S.A. 108 (2011), 13728–13733.
88. [88] Locke, J.A., Guns, E.S., Lubik, A.A., Adomat, H.H., Hendy, S.C., Wood, C.A., Ettinger, S.L., Gleave, M.E., Nelson, C.C., Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer. Cancer Res. 68 (2008), 6407–6415.
89. [89] Culig, Z., Hobisch, A., Cronauer, M.V., Radmayr, C., Trapman, J., Hittmair, A., Bartsch, G., Klocker, H., Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res. 54 (1994), 5474–5478.
90. [90] Yeh, S., Miyamoto, H., Shima, H., Chang, C., From estrogen to androgen receptor: a new pathway for sex hormones in prostate. Proc. Natl. Acad. Sci. U.S.A. 95 (1998), 5527–5532.
91. [91] Zhu, H., Garcia, J.A., Targeting the adrenal gland in castration-resistant prostate cancer: a case for orteronel a selective CYP-17,20-lyase inhibitor. Curr. Oncol. Rep. 15 (2013), 105–112.
92. [92] Taplin, M.E., Bubley, G.J., Shuster, T.D., Frantz, M.E., Spooner, A.E., Ogata, G.K., Keer, H.N., Balk, S.P., Mutation of the androgen-receptor gene in metastatic androgen-independent prostate cancer. N. Engl. J. Med. 332 (1995), 1393–1398.
93. [93] Zhu, M.-L., Kyprianou, N., Role of androgens and the androgen receptor in epithelial-mesenchymal transition and invasion of prostate cancer cells. FASEB J. 24 (2010), 769–777.
94. [94] Chen, M., Chen, L.M., Chai, K.X., Androgen regulation of prostasin gene expression is mediated by sterol-regulatory element-binding proteins and SLUG. The Prostate 66 (2006), 911–920.
95. [95] Shiota, M., Yokomizo, A., Tada, Y., Inokuchi, J., Kashiwagi, E., Masubuchi, D., Eto, M., Uchiumi, T., Naito, S., Castration resistance of prostate cancer cells caused by castration-induced oxidative stress through Twist1 and androgen receptor overexpression. Oncogene 29 (2009), 237–250.
96. [96] Sun, Y., Wang, B.-E., Leong, K.G., Yue, P., Li, L., Jhunjhunwala, S., Chen, D., Seo, K., Modrusan, Z., Gao, W.-Q., Settleman, J., Johnson, L., Androgen deprivation causes epithelial–mesenchymal transition in the prostate: implications for androgen-deprivation therapy. Cancer Res. 72 (2012), 527–536.
97. [97] Singh, A., Settleman, J., EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer. Oncogene 29 (2010), 4741–4751.
98. [98] Matuszak, E.A., Kyprianou, N., Androgen regulation of epithelial-mesenchymal transition in prostate tumorigenesis. Expert Rev. Endocrinol. Metabol. 6 (2011), 469–482.
99. [99] Tannock, I.F., de Wit, R., Berry, W.R., Horti, J., Pluzanska, A., Chi, K.N., Oudard, S., Théodore, C., James, N.D., Turesson, I., Rosenthal, M.A., Eisenberger, M.A., Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. New Engl. J. Med. 351 (2004), 1502–1512.
100. [100] Bullock, M.D., Sayan, A.E., Packham, G.K., Mirnezami, A.H., MicroRNAs: critical regulators of epithelial to mesenchymal (EMT) and mesenchymal to epithelial transition (MET) in cancer progression. Biol. Cell 104 (2012), 3–12 Under the auspices of the European Cell Biology Organization.
101. [101] Gibbons, D.L., Lin, W., Creighton, C.J., Rizvi, Z.H., Gregory, P.A., Goodall, G.J., Thilaganathan, N., Du, L., Zhang, Y., Pertsemlidis, A., Kurie, J.M., Contextual extracellular cues promote tumor cell EMT and metastasis by regulating miR-200 family expression. Genes Dev. 23 (2009), 2140–2151.
102. [102] Korpal, M., Lee, E.S., Hu, G., Kang, Y., The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2. J. Biol. Chem. 283 (2008), 14910–14914.
103. [103] Gregory, P.A., Bert, A.G., Paterson, E.L., Barry, S.C., Tsykin, A., Farshid, G., Vadas, M.A., Khew-Goodall, Y., Goodall, G.J., The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1. Nat. Cell Biol. 10 (2008), 593–601.
104. [104] Park, S.M., Gaur, A.B., Lengyel, E., Peter, M.E., The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2. Genes Dev. 22 (2008), 894–907.
105. [105] Burk, U., Schubert, J., Wellner, U., Schmalhofer, O., Vincan, E., Spaderna, S., Brabletz, T., A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells. EMBO Rep. 9 (2008), 582–589.
106. [106] Brabletz, S., Brabletz, T., The ZEB/miR-200 feedback loop—a motor of cellular plasticity in development and cancer?. EMBO Rep. 11 (2010), 670–677.
107. [107] Liu, Y.N., Yin, J.J., Abou-Kheir, W., Hynes, P.G., Casey, O.M., Fang, L., Yi, M., Stephens, R.M., Seng, V., Sheppard-Tillman, H., Martin, P., Kelly, K., MiR-1 and miR-200 inhibit EMT via Slug-dependent and tumorigenesis via Slug-independent mechanisms. Oncogene 32 (2013), 296–306.
108. [108] Kong, D., Li, Y., Wang, Z., Banerjee, S., Ahmad, A., Kim, H.-R.C., Sarkar, F.H., MiR-200 regulates PDGF-D-mediated epithelial–mesenchymal transition, adhesion, and invasion of prostate cancer cells. Stem Cells 27 (2009), 1712–1721.
109. [109] Waltering, K.K., Porkka, K.P., Jalava, S.E., Urbanucci, A., Kohonen, P.J., Latonen, L.M., Kallioniemi, O.P., Jenster, G., Visakorpi, T., Androgen regulation of micro-RNAs in prostate cancer. Prostate 71 (2011), 604–614.
110. [110] Viticchiè, G., Lena, A.M., Latina, A., Formosa, A., Gregersen, L.H., Lund, A.H., Bernardini, S., Mauriello, A., Miano, R., Spagnoli, L.G., MiR-203 controls proliferation, migration and invasive potential of prostate cancer cell lines. Cell Cycle 10 (2011), 1121–1131.