dc.description.abstract | The present thesis was to test the hypothesis that resistin and leptin differentially regulated the growth between androgen-dependent LNCaP-104S and androgen-independent LNCaP-104R1、LNCaP-104R2 and PC-3 prostate cancer cells, and the hypothesis that endothelin (ET)-1 stimulated the gene expression of suppressors of cytokine signaling (SOCSs) in human prostate cancer cells. At treating 48 hours, resistin generally induced the proliferation (as indicated by an increased number of cells) of LNCaP-104R1、LNCaP-104R2 and PC-3 rather than LNCaP-104S prostate cancer cells. Leptin induced the proliferation of LNCaP-104S、LNCaP-104R1 and PC-3 prostate cancer cells. These data support our first hypothesis. Interestingly, the expression level of the resistin and leptin downstream SOCS genes were different between LNCaP-FGC and PC-3 cells. Although SOCS-1 and SOCS-3 were absent in the LNCaP-FGC cell, all of SOCS family members, such as SOCS-1, -2, -3, -4, -5, -6, and -7 and CIS-1, present in PC-3 cell and U-937 lymphoma cell. The SOCS-3 was also absent in LNCaP-104S、LNCaP-104R1 and LNCaP-104R2 cells. Using PC-3 cell, we found that ET-1 stimulated increases in levels of SOCS-1, -3, and -5 mRNAs in time and dose-dependent manners and had no effects on mRNA levels of other SOCS family members. In addition, treatment of PC-3 cell with green tea epigallocatechin-3-gallate (EGCG) alone induced increases in levels of SOCS-1, -3 and -5 mRNAs and unaltered mRNA expression of other SOCS family members. In the prescence of ET-1, EGCG was interestingly found to inhibit the ET-1 stimulated increases of SOCS-1, -3 and -5 mRNA levels in PC-3 cell. These data suggest that EGCG and ET-1 selectively affects particular types of SOCS family members. As some of SOCSs have been reported to regulate growth of prostate cancer cells, results of this study may help explain the mechanism in the adipokine and ET-1 stimulation of prostate cancer cell growth, as well as the mechanisms of which EGCG suppresses growth of prostate cancer cells. | en_US |