Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Shikonin suppresses the proliferation and colony formation of gastric cancer cells by regulating miR-96/SOCS4 pathway

Peipei Cai, Qingqing Zhang, Zongpin Chen, Fangpeng Ye, Rongzhou Li, Tingting Ji

Department of Digestive System, Ruian People's Hospital (Third Affiliated Hospital of Wenzhou Medical University), Ruian City, Wenzhou, Zhejiang Province 325200, China;

For correspondence:- Tingting Ji Email: TingtingJisrt@163.com Tel:+8657765866161

Accepted: 26 November 2019 Published: 30 December 2019

Citation: Cai P, Zhang Q, Chen Z, Ye F, Li R, Ji T. Shikonin suppresses the proliferation and colony formation of gastric cancer cells by regulating miR-96/SOCS4 pathway. Trop J Pharm Res 2019; 18(12):2479-2485 doi: 10.4314/tjpr.v18i12.3

© 2019 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 whether shikonin is able to inhibit cell proliferation and colony formation in gastric cancer (GC) cells and to elucidate the molecular mechanism.

Methods: Gastric cancer (GC) cell line SGC-7901 was used. The effects of shikonin on SGC-7901 cells were evaluated using Cell Counting Kit-8 (CCK-8) and soft-agar colony formation assays, respectively. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to measure miR-96 expression levels. The regulatory effect of miR-96 on SOCS4 was determined by luciferase activity assay, while the effect of shikonin and miR-96 overexpression on proliferating cell nuclear antigen (PCNA), cyclin D1, suppressor of cytokine signaling 4 (SOCS4), and JAK/STAT pathway-related protein expression levels were analyzed by western blots.

Results: The results show that shikonin dose-dependently suppressed the proliferation and colony formation of SGC-7901 cells. Western blot analysis revealed that PCNA and cyclin D1 were downregulated by shikonin treatment. Luciferase activity assay demonstrated that miR-96 is directly bound to SOCS4. Further results showed that miR-96 mimics reversed the effects of shikonin on SOCS4 and JAK/STAT pathway-related protein expression levels.

Conclusion: Shikonin suppresses proliferation and colony formation by regulating miR-96/SOCS4 pathway in SGC-7901 cells, providing a potential therapeutic target for GC.

Keywords: Shikonin, Gastric cancer, MiR-96, SOCS4