Cytogenetic analysis of four primary prostatic cultures☆
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Cited by (38)
SMILE upregulated by metformin inhibits the function of androgen receptor in prostate cancer cells
2014, Cancer LettersCitation Excerpt :DHT enhanced survival and proliferation of the cells through direct interaction with GR, which formed complex with activated STAT5 [47]. In this study, we showed that metformin inhibited the growth of AR-negative PPC-1 prostate cancer cells, a cell line derived from PC3 [48], in the presence of DHT (Fig. 1A, bottom panel). This metformin-mediated inhibition of cell growth might be due to the reduction of DHT-induced GR expression in PPC-1 cells (Supplemental Fig. S1).
Hepatocyte nuclear factor-3 alpha (HNF-3α) negatively regulates androgen receptor transactivation in prostate cancer cells
2008, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Because AR plays an important role in the proliferation, survival, and differentiation of prostatic cells [5], we attempted to assess the possibility of cross-talk between HNF-3α and AR. We transiently transfected the PPC-1 prostate cancer cell line, an AR-negative PC-3 derivative [4], with the HNF-3α expression construct, and evaluated its effects on AR transactivation. As shown in Fig. 1A, HNF-3α as well as the other family members HNF-3β and HNF-3γ strongly repressed the androgen-dependent expression of the pARE2-TATA-Luc reporter gene.
Deletion (1)(q12) and double minutes in a metastatic adenocarcinoma of the prostate
2000, Cancer Genetics and CytogeneticsStructural alterations of chromosome 5 in twelve human prostate cancer cell lines
1998, Cancer Genetics and CytogeneticsCytogenetic studies in prostate cancer: Are we making progress?
1997, Cancer Genetics and CytogeneticsCombined cytogenetic and molecular genetic analyses of fifty-nine untreated human prostate carcinomas
1996, Cancer Genetics and Cytogenetics
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This work was supported by R01-CA46269 from the National Cancer Institute.