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Tangeretin inhibits hepatocellular carcinoma proliferation and migration by promoting autophagy-related BECLIN1

Authors Zheng J, Shao Y, Jiang Y, Chen F, Liu S, Yu N, Zhang D, Liu X, Zou L

Received 9 January 2019

Accepted for publication 18 April 2019

Published 6 June 2019 Volume 2019:11 Pages 5231—5242

DOI https://doi.org/10.2147/CMAR.S200974

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 3

Editor who approved publication: Dr Chien-Feng Li


Jiao Zheng,1 Yaqin Shao,1 Yu Jiang,2 Fang Chen,2 Sulai Liu,3 Nanhui Yu,2 Dandan Zhang,2 Xiehong Liu,2 Lianhong Zou2

1Drug Clinical Trial Institution Department, Hunan Provincial People’s Hospital, First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, People’s Republic of China; 2Hunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, Changsha, Hunan, People’s Republic of China; 3Hunan Research Center of Biliary Disease, Department of Hepatobiliary Surgery, Hunan Provincial People’s Hospital, Changsha, Hunan, People’s Republic of China

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.

Keywords: hepatocellular carcinoma, Tangeretin, BECLIN1, JNK1

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