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首页> 美国卫生研究院文献>World Journal of Gastroenterology >Inhibition of signal transducer and activator of transcription 3 expression by RNA interference suppresses invasion through inducing anoikis in human colon cancer cells
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Inhibition of signal transducer and activator of transcription 3 expression by RNA interference suppresses invasion through inducing anoikis in human colon cancer cells

机译：RNA干扰抑制信号转导子和转录激活子3的表达通过诱导人类结肠癌细胞的失衡抑制入侵

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AIM: To investigate the roles and mechanism of signal transducer and activator of transcription 3 (STAT3) in invasion of human colon cancer cells by RNA interference.METHODS: Small interfering RNA (siRNA) targeting Signal transducer and activator of transcription 3 (STAT3) was transfected into HT29 colon cancer cells. STAT3 protein level and DNA-binding activity of STAT3 was evaluated by western blotting and electrophoretic mobility shift assay (EMSA), respectively. We studied the anchorage-independent growth using colony formation in soft agar, and invasion using the boyden chamber model, anoikis using DNA fragmentation assay and terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL), respectively. Western blot assay was used to observe the protein expression of Bcl-xL and survivin in colon cancer HT29 cells.RESULTS: RNA interference (RNAi) mediated by siRNA leads to suppression of STAT3 expression in colon cancer cell lines. Suppression of STAT3 expression by siRNA could inhibit anchorage-independent growth, and invasion ability, and induces anoikis in the colon cancer cell line HT29. It has been shown that knockdown of STAT3 expression by siRNA results in a reduction in expression of Bcl-xL and survivin in HT29 cells.CONCLUSION: These results suggest that STAT3 siRNA can inhibit the invasion ability of colon cancer cells through inducing anoikis, which antiapoptotic genes survivin and Bcl-xL contribute to regulation of anoikis. These studies indicate STAT3 siRNA could be a useful therapeutic tool for the treatment of colon cancer.
机译：目的：探讨信号转导和转录激活因子（STAT3）在RNA干扰下侵袭人结肠癌细胞的作用和机制。方法：针对小干扰RNA（siRNA）靶向信号转导和转录激活因子（STAT3）转染到HT29结肠癌细胞中。 STAT3蛋白水平和STAT3的DNA结合活性分别通过蛋白质印迹和电泳迁移率变动分析（EMSA）进行评估。我们分别研究了在软琼脂上使用集落形成的锚定非依赖性生长，并使用博伊登室模型研究了侵袭，使用DNA片段化分析和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）进行了无神经生长。结果：siRNA介导的RNA干扰（RNAi）可抑制结肠癌细胞株STAT3的表达。Westernblot法可检测Bcl-xL和survivin在结肠癌HT29细胞中的表达。 siRNA抑制STAT3的表达可抑制锚定非依赖性生长和侵袭能力，并在结肠癌细胞株HT29中诱导失神经。 siRNA抑制STAT3表达可导致HT29细胞中Bcl-xL和survivin表达降低。结论：STAT3 siRNA可通过诱导凋亡诱导的凋亡来抑制结肠癌细胞的侵袭能力。 survivin和Bcl-xL基因有助于调节无神经。这些研究表明STAT3 siRNA可能是治疗结肠癌的有用治疗工具。

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