Steiner M S
Department of Urology and Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
World J Urol. 1995;13(6):329-36. doi: 10.1007/BF00191213.
This review focuses on the possible role of transforming growth factor-beta isoforms 1-3 (TGFbeta) in prostate cancer. TGFbeta1 appears to inhibit the cellular proliferation of normal prostate cells. Surprisingly, TGFbeta1 is overexpressed in prostate cancer. To help explain this apparent paradox, it has been revealed that with tumor progression, prostate cancer cells acquire reduced sensitivity to the growth-inhibitory effects of TGFbeta1. Aberrations of the TGFbeta1 signaling pathway at the prereceptor, receptor, or postreceptor level may lead to prostate cancer cell resistance to TGFbeta1 growth inhibition. Indirectly, elevated levels of TGFbeta1 may induce host effects that may be beneficial to prostate tumor growth by suppressing the immune system, promoting angiogenesis and extracellular matrix formation, and enhancing metastatic potential. Consequently, TGFbeta1 appears to be important in prostate carcinogenesis and tumorigenicity. TGFbeta2 and TGFbeta3 are only briefly presented as very little is known about their role in prostate cancer.
本综述聚焦于转化生长因子-β亚型1-3(TGFβ)在前列腺癌中可能发挥的作用。TGFβ1似乎可抑制正常前列腺细胞的增殖。令人惊讶的是,TGFβ1在前列腺癌中过度表达。为解释这一明显的矛盾现象,研究发现随着肿瘤进展,前列腺癌细胞对TGFβ1的生长抑制作用敏感性降低。TGFβ1信号通路在前受体、受体或受体后水平的异常可能导致前列腺癌细胞对TGFβ1生长抑制产生抗性。间接而言,TGFβ1水平升高可能通过抑制免疫系统、促进血管生成和细胞外基质形成以及增强转移潜能,诱导对前列腺肿瘤生长有益的宿主效应。因此,TGFβ1在前列腺癌发生和致瘤性方面似乎很重要。由于对TGFβ2和TGFβ3在前列腺癌中的作用了解甚少,故仅作简要介绍。