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Original Research Article | OPEN ACCESS

Jatrorrhizine inhibits liver cancer cell growth by targeting the expressions of miR-221-3p and miR-15b-5p

Bo Deng1, Maolin Wan2

1Department of Oncology, Xianning Central Hospital, Xianning 431700; 2Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Hubei University of science and technology, Hubei 437199, China.

For correspondence:-  Maolin Wan   Email: wn47935142@163.com   Tel:+867158236000

Accepted: 23 July 2021        Published: 31 August 2021

Citation: Deng B, Wan M. Jatrorrhizine inhibits liver cancer cell growth by targeting the expressions of miR-221-3p and miR-15b-5p. Trop J Pharm Res 2021; 20(8):1573-1578 doi: 10.4314/tjpr.v20i8.4

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of jatrorrhizine on hepatic cancer cell proliferation and its mechanism of action.
Methods: Jatrorrhizine-mediated changes in cell viability were measured using (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while apoptosis induction was evaluated by flow cytometry. Transwell assay was used for the measurement of cell invasion, whereas cell migration was assessed by wound healing assay. The protein expression of Axin2 was determined with western blotting assay.
Results: Jatrorrhizine significantly (p < 0.049) suppressed the viability of HepG2 and HCCLM3 cells in the concentration range of 0.5 to 16.0 µM. Treatment of HepG2 and HCCLM3 cells with 4.0 µM jatrorrhizine markedly suppressed cell invasion, when compared to untreated cells (p < 0.0493). Jatrorrhizine significantly promoted the apoptosis of HepG2 and HCCLM3 cells at 48 h, relative to untreated cells, but 16.0 µM jatrorrhizine markedly suppressed the expressions of miR?221?3p and miR?15b?5p (p < 0.0493). Moreover, jatrorrhizine significantly up-regulated the protein expressions of Axin2 in HepG2 and HCCLM3 cells at 48 h (p < 0.0493).
Conclusion: Jatrorrhizine inhibits the proliferation, and suppressed the invasiveness and migration of HepG2 and HCCLM3 liver cancer cells, but increases their apoptosis. Moreover, it down-regulates the expressions of miR-221-3p and miR15b-5p and promotes Axin2 protein expression in HepG2 and HCCLM3 cells. Therefore, jatrorrhizine is a potential drug candidate for the treatment of liver cancer.

Keywords: Jatrorrhizine, Liver cancer, HepG2, HCCLM3, Apoptosis, Axin2, MiR?221?3p, MiR?15b?5p

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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