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首页> 外文期刊>Molecular cancer research: MCR >Exogenous Fibroblast Growth Factors Maintain Viability, Promote Proliferation, and Suppress GADD45{alpha} and GAS6 Transcript Content of Prostate Cancer Cells Genetically Modified to Lack Endogenous FGF-2.
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Exogenous Fibroblast Growth Factors Maintain Viability, Promote Proliferation, and Suppress GADD45{alpha} and GAS6 Transcript Content of Prostate Cancer Cells Genetically Modified to Lack Endogenous FGF-2.

机译：外源成纤维细胞生长因子维持活力，促进增殖并抑制经遗传修饰为缺乏内源性FGF-2的前列腺癌细胞的GADD45 {α}和GAS6转录物含量。

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Understanding processes regulating prostate cancer cell survival is critical to management of advanced disease. We used prostate cancer cell transfectants genetically modified to be deficient in either endogenous fibroblast growth factor (FGF-1) or endogenous FGF-2 to examine FGF maintenance of transfectant survival and proliferation and FGF-2-regulated expression of transfectant growth arrest DNA damage (GADD) and growth arrest sequences (GAS) family genes (known modulators of cell cycle progression and survival) and the AS3 gene (an androgen-modulated effector of prostate cell proliferation). When propagated in the absence of exogenous FGFs, FGF-2-deficient transfectants undergo exponential death, whereas FGF-1-deficient transfectants proliferate. Exogenous FGF-1, FGF-2, FGF-7, or FGF-8 promote survival and proliferation of FGF-2-deficient transfectants and enhance FGF-1-deficient transfectant proliferation. Transfectants express FGF receptor FGFR1, FGFR2(IIIb), FGFR2(IIIc), and FGFR3 transcripts, findings consistent with the effects of exogenous FGFs. FGF-2-deficient transfectants express high levels of AS3, GADD45alpha, GADD45gamma, GAS8, and GAS11 transcripts and moderate levels of GADD153, GAS2, GAS3, and GAS6 transcripts and lack demonstrable GAS1 or GAS5 transcripts. FGF withdrawal-mediated death of FGF-2-deficient transfectants did not significantly affect cell AS3, GADD153, GADD45gamma, GAS2, GAS3, GAS7, GAS8, or GAS11 transcript content, whereas GADD45alpha and GAS6 transcript content was elevated. These studies establish that endogenous FGF-2 dominantly regulates prostate cancer cell survival and proliferation and that exogenous FGFs may assume this function in the absence of endogenous FGF-2. Additionally, we provide the first evidence that FGFs regulate prostate GADD45alpha and GAS6 transcript content. The latter observations suggest that GADD45alpha and GAS6 proteins may be effectors of processes that regulate prostate cancer cell survival. Additional studies are required to examine this possibility in detail.
机译：了解调节前列腺癌细胞存活的过程对于晚期疾病的治疗至关重要。我们使用经过基因改造以缺乏内源性成纤维细胞生长因子（FGF-1）或内源性FGF-2的前列腺癌细胞转染子来检查FGF维持转染子存活和增殖以及FGF-2调控的转染子生长停滞DNA损伤的表达（ GADD）和生长停滞序列（GAS）家族基因（已知的细胞周期进程和存活调节剂）和AS3基因（雄激素调节的前列腺细胞增殖效应子）。当在没有外源FGF的情况下繁殖时，缺乏FGF-2的转染子将经历指数死亡，而缺乏FGF-1的转染子会增殖。外源FGF-1，FGF-2，FGF-7或FGF-8促进FGF-2缺陷型转染子的存活和增殖，并增强FGF-1缺陷型转染子的增殖。转染子表达FGF受体FGFR1，FGFR2（IIIb），FGFR2（IIIc）和FGFR3转录本，这些发现与外源FGF的作用一致。缺乏FGF-2的转染子表达高水平的AS3，GADD45alpha，GADD45gamma，GAS8和GAS11转录本，中等水平的GADD153，GAS2，GAS3和GAS6转录本，并且缺乏可证明的GAS1或GAS5转录本。 FGF退出介导的FGF-2缺陷转染子的死亡并未显着影响细胞AS3，GADD153，GADD45gamma，GAS2，GAS3，GAS7，GAS8或GAS11转录物含量，而GADD45alpha和GAS6转录物含量升高。这些研究证实，内源性FGF-2主要调节前列腺癌细胞的存活和增殖，并且在不存在内源性FGF-2的情况下，外源性FGFs可以发挥这种功能。此外，我们提供了FGF调节前列腺GADD45alpha和GAS6转录物含量的第一个证据。后面的观察结果表明，GADD45alpha和GAS6蛋白可能是调节前列腺癌细胞存活的过程的效应子。需要进行其他研究以详细研究这种可能性。

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