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Diosmetin Inhibits Cell Proliferation, Induces Cell Apoptosis and Cell Cycle Arrest in Liver Cancer

Authors Ma A, Zhang R

Received 26 November 2019

Accepted for publication 8 April 2020

Published 18 May 2020 Volume 2020:12 Pages 3537—3546

DOI https://doi.org/10.2147/CMAR.S240064

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly


Aiqing Ma,1 Rui Zhang2

1Department of Operating Room, Linyi Cancer Hospital, Linyi, Shandong, People’s Republic of China; 2Department of Thoracic Surgery, Linyi Cancer Hospital, Linyi, Shandong, People’s Republic of China

Correspondence: Rui Zhang
Department of Thoracic Surgery, Linyi Cancer Hospital, Linyi, Shandong 276001, People’s Republic of China
Email Zhangruidoctor123@163.com

Objective: Diosmetin (DIOS) has been confirmed to possess anti-cancer effects in some types of tumors. However, it remains unclear whether DIOS exerts anti-cancer effects on liver cancer. Thus, our purpose was to observe the effect of DIOS on cell proliferation, cell apoptosis and cell cycle arrest in human liver cancer cells.
Materials and Methods: The cell viability of HepG2 and HCC-LM3 cells under different concentrations of DIOS was detected using MTT assay. The cell apoptosis and cell cycle arrest were analyzed by flow cytometry. The expression levels of apoptosis/cell cycle-related proteins including P53, Bcl-2, Bax, cleaved-caspase3, cleaved-caspase8, cleaved-PARP, Bak, cdc2, cyclinB1 and P21 were measured using Western blot. HepG2 cells were transfected by checkpoint kinase 1 (Chk1)-small interfering RNA (siRNA) and checkpoint kinase 2 (Chk2)-siRNA, respectively. After that, cell cycle was detected.
Results: DIOS significantly suppressed cell proliferation and induced cell apoptosis of HepG2 cells and HCC-LM3 cells. Moreover, DIOS promoted cell cycle arrest in G2/M phase. Western blot results showed that DIOS significantly suppressed the expression levels of Bcl-2, cdc2, cyclinB1, and promoted the expression levels of Bax, cleaved-caspase3, cleaved-caspase8, cleaved-PARP, Bak, P53, and P21. The G2/M phase arrest was observed in HepG2 cells transfected with Chk2-siRNA, while the G2/M phase arrest was not obvious in HepG2 cells transfected with Chk1-siRNA.
Conclusion: Our findings revealed that DIOS could inhibit cell proliferation and promote cell apoptosis and cell cycle arrest in liver cancer. Furthermore, DIOS could induce G2/M cell cycle arrest in HepG2 cell via targeting Chk2.

Keywords: diosmetin, cell apoptosis, cell cycle arrest, liver cancer, HepG2 cell


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