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SMAD-4在肿瘤抑制方面有重要作用,但它在肿瘤发生中的作用及其与细胞周期进程中的一种关键调控因子——PTEN(phosphatase and tensin homolog deleted on chromosome 10)的关系仍存在争议.分别在人胚肾细胞(293T)及人胃癌细胞(MGC-803)中研究SMAD-4及TGF-β信号通路对PTEN基因表达的影响.结果发现,在293T细胞中,SMAD-4与TGF-β促进PTEN表达,而MGC-803细胞中,SMAD-4与TGF-β抑制PTEN转录.进一步研究发现,胃癌细胞中,SMAD-4与转化生长因子β(TGF-β)对PTEN的抑制可被PD98059(MEK抑制剂)解除.此外,SMAD-4的核转移也明显促进PTEN表达,并且PD98059存在下,SMAD-4与TGF-β协同刺激可促进胃癌细胞凋亡.综上,实验发现,SMAD-4作为一种co-Smad蛋白,通过TGF-β信号途径影响PTEN表达.
Although SMAD-4 plays an important role in tumor suppression, its role in tumorigenesis and its relationship with PTEN (phosphatase and tensin homolog deleted on chromosome 10) remain controversial The effects of SMAD-4 and TGF-β signaling on the expression of PTEN gene were studied in human embryonic kidney (293T) and human gastric cancer cells (MGC-803) -βpromoted the expression of PTEN, but SMAD-4 and TGF-β inhibited PTEN transcription in MGC-803 cells.Further study found that the inhibition of PTEN by SMAD-4and TGF-βcan be inhibited in gastric cancer cells In addition, SMAD-4 nuclear transfer also significantly promote the expression of PTEN, and in the presence of PD98059, SMAD-4 and TGF-β synergistic stimulation can promote gastric cancer cell apoptosis.In summary, the experiment found that, SMAD-4, a co-Smad protein, affects PTEN expression through the TGF-β signaling pathway.