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Original Research Article | OPEN ACCESS

Silencing of acetyl-CoA carboxylase-α gene in human gastric cancer cells inhibits proliferation via induction of apoptosis, autophagy and suppression of cell invasion

Chunsong Yu1, Xuehong Wu1, Bihua Yao1, Huaxing Tao2

1Clinical Laboratory, The First People's Hospital of Jiashan; 2Department of Infection, The First People's Hospital of Jiashan County, Zhejiang Province 314100, China.

For correspondence:-  Huaxing Tao   Email: HongMclaughlinbmh@yahoo.com   Tel:+8657384039637

Accepted: 24 September 2019        Published: 30 October 2019

Citation: Yu C, Wu X, Yao B, Tao H. Silencing of acetyl-CoA carboxylase-α gene in human gastric cancer cells inhibits proliferation via induction of apoptosis, autophagy and suppression of cell invasion. Trop J Pharm Res 2019; 18(10):2025-2030 doi: 10.4314/tjpr.v18i10.4

© 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 study the role and therapeutic potential of acetyl-CoA-carboxylase-α (ACC) in the management of gastric cancer. 
Methods: expression of ACC in gastric cancer cell lines was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used for transfection, while cell viability was determined by MTT assay. Apoptotic cell death was assayed with 4′, 6-diamidino-2-phenylindole (DAPI) and acridine orange/ethidium bromide (AO/EB) staining. The proportion of apoptotic cells was estimated with Annexin V/PI staining. Wound healing and Transwell assays were employed to monitor cell migration and invasion, while protein expression was determined using western blotting.
Results: The results showed that ACC was significantly enhanced in SNU-1 gastric cancer cells (4.2-fold). Silencing of ACC in SNU-1 gastric cancer cells caused significant decrease in cell proliferation (p < 0.05). Electron microscopy examination showed that ACC silencing triggered autophagic cell death in SNU-1 cells, and increased expression of LC3 II. Results from DAPI and AO/EB assays demonstrated that ACC silencing also promoted apoptosis in SNU-1 gastric cancer cells. Annexin V/PI assay results revealed that apoptotic cell population increased from 2.7 to 13.8 % due to ACC silencing (p < 0.05). Moreover, Bax expression increased, while Bcl-2 expression decreased upon ACC silencing. Transwell assay results indicate that ACC silencing caused marked decrease in the invasion of the SNU-1 cells and downregulation of the expressions of MMP-2 and MMP-9 (p < 0.05).
Conclusion: ACC is likely to be an important therapeutic target for gastric cancer.

Keywords: Gastric cancer, Acetyl-CoA-carboxylase-^5;, Apoptosis, Invasion, Autophagy

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

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