Tangeretin inhibits hepatocellular carcinoma proliferation and migration by promoting autophagy-related BECLIN1 (Retracted Article)
Tangeretin inhibits hepatocellular carcinoma proliferation and migration by promoting autophagy-related BECLIN1 (Retracted Article)
复制标题
橘皮素通过促进自噬相关的BECLIN1抑制肝细胞癌的增殖和迁移
DOI：
10.2147/cmar.s200974
复制
发表时间：
2019-01-01
影响因子：
3.3
通讯作者：
Zou, Lianhong
中科院分区：
文献类型：
--
作者：
Zheng, Jiao;Shao, Yaqin;Zou, Lianhong
背景：肝细胞癌（HCC）是一种特别普遍的肝癌类型，是亚洲最致命的恶性肿瘤之一。橘皮素是一种从传统中草药中提取的生物化合物，已被证明具有潜在的抗肿瘤特性；然而，其机制在很大程度上仍然未知。因此，我们试图确定橘皮素在接受抗肿瘤治疗的HepG2细胞中的作用。材料和方法：用CCK-8、EdU和菌落形成法定量细胞增殖，用transwell迁移法和伤口愈合法定量细胞迁移。Western blot检测蛋白表达。用小干扰RNA干扰蛋白表达。免疫沉淀法检测蛋白-蛋白相互作用。结果：橘皮素抑制细胞增殖，提高G2/M阻滞。橘皮素减少细胞迁移。橘皮素增加HepG2细胞LC3II/LC3I比值，降低p62表达。此外，在HepG2细胞中，BECLIN1表达的下调部分转化了橙皮素诱导的增殖、迁移和自噬的抑制。此外，橘皮素激活JNK1/Bcl-2通路，干扰Bcl-2与BECLIN1的相互作用。总之，我们的研究结果表明，橘皮素通过JNK/Bcl-2/BECLIN1途径介导的自噬抑制HepG2细胞的增殖和迁移。结论：我们的研究有助于理解橙皮素对HCC发展的抑制机制。
Background: Hepatocellular carcinoma (HCC) is a particularly prevalent type of liver cancer and is one of the deadliest malignancies in Asia. Tangeretin is a biological compound extracted from traditional Chinese herbs and has been shown to have potential antitumour properties; however, its mechanism remains largely unknown. Therefore, we sought to determine the role of Tangeretin in HepG2 cells subjected to antitumour treatment. Materials and methods: Cell proliferation was quantified using CCK-8, EdU and colony formation assays, and cell migration was quantified using transwell migration and wound healing assays. Protein expression was assessed using Western blot analysis. Small interfering RNA was used to interfer protein expression. Immunoprecipitation was performed to detect the protein-protein interactions. Results: Tangeretin decreased cell proliferation and increased G2/M arrest. Tangeretin decreased cell migration. Tangeretin increased the LC3II/LC3I ratio and decreased p62 expression in HepG2 cells. Furthermore, the knockdown of BECLIN1 expression in HepG2 cells partially converted the Tangeretin-induced inhibition of proliferation, migration and autophagy. In addition, Tangeretin activated the JNK1/Bcl-2 pathway and disturbed the interaction between Bcl-2 and BECLIN1. Together, our findings demonstrate that Tangeretin inhibited the proliferation and migration of HepG2 cells through JNK/Bcl-2/BECLIN1 pathway-mediated autophagy. Conclusion: Our study contributes to the understanding of the inhibitory mechanism of Tangeretin on HCC development.