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- W2981810904 abstract "1943 Previous work from this laboratory has demonstrated that a molecular mimic of naturally phosphorylated prolactin, S179D PRL, inhibited cell growth in several human prostate cancer lines in vitro and the growth of DU145 cells when grown as tumors in nude mice (Cancer Res 61:6098,2001). In part, the growth inhibition is by blockade of an autocrine unmodified prolactin (U-PRL) growth loop working through the long PRL receptor, but several lines of data suggest additional mechanisms. In this study, we have further investigated the molecular mechanism of this growth inhibition by comparing the more differentiated, lower autocrine U-PRL-producing LnCAP cell line with the less differentiated, higher autocrine U-PRL-producing DU145 cell line. LnCAP and DU145 cells were grown in RPMI 1640 supplemented with 10% fetal bovine serum (FBS) or 10% charcoal-stripped FBS and, when confluent, were treated with 1 μg/ml U-PRL, S179D PRL or diluent for 3 days (daily medium change). Response to S179D PRL differed between the two cell lines. In the LnCAP cells, but not the DU145 cells, S179D PRL, but not U-PRL, had a long term effect on the activation of ERKs 1 and 2 (>5 fold at 3 days)and upregulated the expression of the vitamin D receptor (VDR) (3 fold, p" @default.
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- W2981810904 date "2004-04-01" @default.
- W2981810904 modified "2023-09-28" @default.
- W2981810904 title "Transfection of human prostate cancer cells (DU145) with the human short prolactin receptor sensitizes the cells to cell cycle regulation by S179D prolactin" @default.
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