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片仔癀通过上调miR-16的表达来抑制肝癌细胞的生长。

Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR-16 expression.

作者信息

Qi Fei, Zhou Songqiang, Li Li, Wei Lihui, Shen Aling, Liu Liya, Wang Yaodong, Peng Jun

机构信息

Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

出版信息

Oncol Lett. 2017 Dec;14(6):8132-8137. doi: 10.3892/ol.2017.7240. Epub 2017 Oct 20.

Abstract

Hepatocellular carcinoma (HCC) is characterized by uncontrolled proliferation and the deregulation of apoptotic signaling, although its molecular pathogenesis is not fully characterized. The ability to inhibit excessive proliferation and induce the apoptosis of cancer cells are crucial characteristics of anticancer drugs. Pien Tze Huang (PZH) is a widely used traditional Chinese medicine for the treatment of various types of cancer, and has exhibited promising therapeutic effects in clinical trials of HCC. However, the underlying mechanisms for its action are unclear. In the present study, the aim was to explore the effect of PZH on the proliferation and apoptosis of the BEL-7402 HCC cell line, and the associated mechanisms. PZH treatment significantly inhibited BEL-7402 cell viability, confluence and clonogenicity, inducing cell cycle arrest and promoting apoptosis. In addition, PZH treatment suppressed the expression of the pro-proliferative genes cyclin D1 and cyclin-dependent kinase 4, and decreased the expression of the anti-apoptotic gene Bcl-2. PZH treatment also upregulated the expression of a key microRNA (miR), miR-16. The study demonstrated that PZH can effectively inhibit cancer cell proliferation and induce apoptosis in BEL-7402 HCC cells via the upregulation of the tumor suppressor miR-16.

摘要

肝细胞癌(HCC)的特征是不受控制的增殖和凋亡信号失调,尽管其分子发病机制尚未完全明确。抑制癌细胞过度增殖和诱导其凋亡的能力是抗癌药物的关键特性。片仔癀(PZH)是一种广泛用于治疗各类癌症的传统中药,并且在HCC的临床试验中已展现出有前景的治疗效果。然而,其作用的潜在机制尚不清楚。在本研究中,目的是探究PZH对BEL-7402肝癌细胞系增殖和凋亡的影响以及相关机制。PZH处理显著抑制了BEL-7402细胞的活力、汇合度和克隆形成能力,诱导细胞周期停滞并促进凋亡。此外,PZH处理抑制了促增殖基因细胞周期蛋白D1和细胞周期蛋白依赖性激酶4的表达,并降低了抗凋亡基因Bcl-2的表达。PZH处理还上调了关键微小RNA(miR)即miR-16的表达。该研究表明,PZH可通过上调肿瘤抑制性miR-16有效抑制BEL-7402肝癌细胞的增殖并诱导其凋亡。

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