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Tanshinone IIA inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cells via p53-cyclin B1/CDC2

机译:丹参酮IIA通过p53细胞周期蛋白B1 / CDC2抑制人鼻咽癌细胞的增殖并诱导其凋亡

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摘要

Tanshinone IIA exhibits natural antioxidative and antineoplastic activity. However, to the best of our knowledge, the effects of tanshinone IIA on human nasopharyngeal carcinoma cells remains unknown. The present study aimed to investigate whether tanshinone IIA inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cells via p53-cyclin B1/cell division cycle gene 2 (CDC2). Cell proliferation, cytotoxicity and apoptosis of 13-9B cells were evaluated by an MTT assay, lactate dehydrogenase assay and flow cytometry, respectively. ELISA and western blot analysis were used to analyze caspase-3 activity and poly (ADP-ribose) polymerase (PARP), p53, cyclin B1 and CDC2 protein expression in 13-9B cells. Treatment of 13-9B cells with tanshinone IIA significantly suppressed cell proliferation and significantly induced cytotoxicity and apoptosis of 13-9B cells. Furthermore, tanshinone IIA significantly increased caspase-3 activity, and significantly increased the protein expression levels of PARP, p53, cyclin B1 and CDC2 in 13-9B cells. In summary, the current results indicate that tanshinone IIA inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cells via PARP, p53, cyclin B1/CDC2 and caspase-3-mediated signaling.
机译:丹参酮IIA具有天然的抗氧化和抗肿瘤活性。然而,就我们所知,丹参酮IIA对人鼻咽癌细胞的作用仍然未知。本研究旨在探讨丹参酮IIA是否通过p53细胞周期蛋白B1 /细胞分裂周期基因2(CDC2)抑制人鼻咽癌细胞的增殖并诱导其凋亡。通过MTT法,乳酸脱氢酶法和流式细胞术分别评估13-9B细胞的细胞增殖,细胞毒性和凋亡。 ELISA和Western blot分析用于分析caspase-3活性和聚(ADP-核糖)聚合酶(PARP),p53,cyclin B1和CDC2蛋白在13-9B细胞中的表达。丹参酮IIA处理13-9B细胞可显着抑制细胞增殖,并显着诱导13-9B细胞的细胞毒性和凋亡。此外,丹参酮IIA显着提高了caspase-3活性,并显着提高了13-9B细胞中PARP,p53,cyclin B1和CDC2的蛋白表达水平。总之,当前结果表明丹参酮IIA通过PARP,p53,细胞周期蛋白B1 / CDC2和caspase-3介导的信号传导抑制人鼻咽癌细胞的增殖并诱导其凋亡。

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