Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

TRIM 16 gene expression regulates the growth and metastasis of human esophageal cancer

Yufang Chen, Ziyan Li, Jingyao Zeng, Zhiyi Xu, Meihua Wang

Department of Pathology, Changzhou Tumor Hospital Affiliated to Soochow University, Changzhou, Jiangsu 213032, China;

For correspondence:- Meihua Wang Email: BartLynnuLcP@yahoo.com Tel:+8651969807262

Accepted: 23 September 2020 Published: 30 October 2020

Citation: Chen Y, Li Z, Zeng J, Xu Z, Wang M. TRIM 16 gene expression regulates the growth and metastasis of human esophageal cancer. Trop J Pharm Res 2020; 19(10):2047-2053 doi: 10.4314/tjpr.v19i10.4

© 2020 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 tripartite membrane protein (TRIM) 16 gene silencing on human esophageal cancer (KYSE-270) cell proliferation, invasion and metastasis.

Methods: Short interfering RNA (siRNA) TRIM 16 silencing fragment was transfected into KYSE-270 cells. Transfection efficiency was determined using real-time quantitative polymerase chain reaction (qRT-PCR). Cell proliferation, invasiveness and migration were measured by 3-(4,5-dimethylthiazol2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, Transwell invasion assay, and scratch test, respectively. Protein expressions of bax and bcl-2 were assayed using Western blotting.

Results: The gene expression of TRIM 16 was significantly upregulated in esophageal cancer cells, relative to normal human esophageal cells, but was downregulated after gene silencing. Moreover, the silencing of TRIM 16 gene led to significant reductions in KYSE-270 cell viability, migration and invasiveness, but significantly increased KYSE270 cell apoptosis (p < 0.05). The silencing of TRIM 16 gene also significantly upregulated bax protein expression, while downregulating the expression of bcl-2 protein (p < 0.05).

Conclusion: These results suggest that TRIM 16 gene silencing inhibits KYSE-270 cell proliferation, invasion and metastasis, and thus provide a basis for its development as a therapeutic approach for the management of esophageal cancer.

Keywords: Apoptosis, Cell invasion, Esophageal cancer, Gene silencing, Metastasis