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Silencing Sirtuin 6 induces cell cycle arrest and apoptosis in non-small cell lung cancer cell lines

机译:沉默的Sirtuin 6在非小细胞肺癌细胞系中诱导细胞周期骤停和细胞凋亡

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Sirtuins (SIRT1–7), are NAD-dependent deacetylases and ADP-ribosyl transferases, plays a major part in carcinogenesis. The previous report suggests that in cancer, sirtuins gained tremendous interest and critical regulators of the unusual processes. In carcinogenesis, sirtuins possess either tumor suppressor or promoter. However, in lung cancer condition the studies of sirtuins are less studied. Hence, this designed study investigates the impact of multifaceted sirtuins in NSCLC cells. We evaluated the mRNA and protein expressions of sirtuins by RTPCR and western blot. We found SIRT6 significantly overexpressed in NCI-H520, A549, and NCI-H460 compared with the normal BEAS-2B cell line. Silencing of SIRT6 by siRNA in NSCLC cells caused activation of p53/p21 mediated inhibition of cell proliferation leading to arrest in cell cycle and apoptosis induction. Our results implied that SIRT6 is a tumor promoter in NSCLC development, progression, and regulation. The silencing of SIRT6 to be a novel therapy for lung cancer.
机译:SIRTUINS(SIRT1-7)是NAD依赖性的脱乙酰酶和ADP-核糖基转移酶,在致癌物中发挥重要作用。之前的报告表明,在癌症中,SIRTUIN获得了不寻常的进程的巨大兴趣和临界监管机构。在癌发生中,SIRTUIN具有肿瘤抑制或启动子。然而,在肺癌条件下,SIRTUIN的研究较少研究。因此,这项设计的研究研究了多方面SIRTUIN在NSCLC细胞中的影响。我们通过RTPCR和Western印迹评估了SIRTUIN的mRNA和蛋白表达。与普通的BEA-2B细胞系相比,我们发现SIRT6在NCI-H520,A549和NCI-H460中显着过表达。 NSCLC细胞中SiRT6的Sirt6沉默引起了P53 / P21介导的细胞增殖抑制的激活,导致细胞周期和凋亡诱导。我们的结果暗示SIRT6是NSCLC发育,进展和监管中的肿瘤启动子。 SIRT6的沉默成为肺癌的新疗法。

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