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.

中文翻译：

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沉默 Sirtuin 6 在非小细胞肺癌细胞系中诱导细胞周期停滞和细胞凋亡。

Sirtuins (SIRT1-7) 是 NAD 依赖性脱乙酰酶和 ADP-核糖基转移酶，在致癌作用中起主要作用。之前的报告表明，在癌症中，sirtuins 获得了极大的兴趣和异常过程的关键调节剂。在致癌作用中，sirtuins 具有肿瘤抑制因子或启动子。然而，在肺癌情况下，sirtuins 的研究较少。因此，这项设计的研究调查了多方面的 Sirtuins 在 NSCLC 细胞中的影响。我们通过 RTPCR 和蛋白质印迹评估了 Sirtuins 的 mRNA 和蛋白质表达。我们发现与正常 BEAS-2B 细胞系相比，SIRT6 在 NCI-H520、A549 和 NCI-H460 中显着过表达。在 NSCLC 细胞中通过 siRNA 沉默 SIRT6 引起 p53/p21 介导的细胞增殖抑制的激活，从而导致细胞周期停滞和细胞凋亡诱导。我们的结果表明 SIRT6 是 NSCLC 发展、进展和调节的肿瘤启动子。SIRT6 的沉默成为肺癌的新疗法。