论文部分内容阅读
目的:探讨STAT3在双酚A促乳腺癌MCF-7细胞增殖中的作用,为研究双酚A诱导乳腺癌的确切机制提供依据。方法:采用Western blot检测双酚A处理乳腺癌MCF-7细胞24 h和48 h后STAT3的表达情况,采用MTT法检测RNA干扰技术抑制STAT3后双酚A对乳腺癌细胞增殖的影响。结果:Western blot结果表明,STAT3在1μM双酚A作用48 h后其诱导表达最明显(P<0.05);通过对照研究筛选出有效的干扰片段,能显著抑制STAT3基因的表达,当干扰片段抑制了STAT3基因表达后,双酚A未能抑制STAT3的MCF-7细胞发生增殖效应(P>0.05)。结论:在双酚A诱导乳腺癌细胞的增殖作用中,STAT3的活化和活化后的信号传导是非常重要的一个环节。
OBJECTIVE: To investigate the role of STAT3 in the proliferation of breast cancer MCF-7 cells induced by bisphenol A, and to provide a basis for studying the exact mechanism of BPA-induced breast cancer. Methods: Western blot was used to detect the expression of STAT3 in breast cancer MCF-7 cells treated with BPA for 24 h and 48 h. The effect of BPA on the proliferation of breast cancer cells was detected by MTT assay. Results: The result of Western blot showed that the STAT3 expression was most obvious at 48 h after treated with 1 μM bisphenol A (P <0.05). The effective interference fragment was screened by the control study, which could significantly inhibit the STAT3 gene expression, After STAT3 gene expression, bisphenol A failed to inhibit the proliferation of STAT3 MCF-7 cells (P> 0.05). CONCLUSION: Activation of STAT3 and signal transduction after activation are important links in the proliferation of breast cancer cells induced by BPA.