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酰基辅酶 A 合成酶 5 促进结直肠癌细胞的生长和侵袭。

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells.

机构信息

Department of Gastroenterology, The First Affiliated Hospital, Shenzhen University, Shenzhen 518035, China.

Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, China.

出版信息

Can J Gastroenterol Hepatol. 2017;2017:7615736. doi: 10.1155/2017/7615736. Epub 2017 Jul 20.

Abstract

BACKGROUND AND AIMS

Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC.

METHODS

ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro.

RESULTS

We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44.

CONCLUSIONS

Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

摘要

背景与目的

酰基辅酶 A 合成酶 5(ACS5)已被报道与多种癌症的发生发展相关,但 ACS5 在结直肠癌(CRC)中的作用尚不清楚。本研究旨在探讨 ACS5 在 CRC 发生发展中的潜在作用。

方法

检测 ACS5 在 CRC 组织和 CRC 细胞系中的表达,并分析其临床意义。体外研究 ACS5 对细胞增殖、凋亡和侵袭的作用。

结果

我们发现 ACS5 在 CRC 细胞和组织中表达上调,且 ACS5 高表达更常见于肌层过度浸润和肿瘤分化差的 CRC 患者。此外,在 HT29 和 SW480 细胞中敲低 ACS5 显著抑制细胞增殖,诱导细胞凋亡,并减少细胞迁移和侵袭。相反,在 LOVO 和 SW620 细胞中过表达 ACS5 则显著促进细胞增殖,抑制细胞凋亡,并增强细胞迁移和侵袭。ACS5 表达增加介导的细胞生长和侵袭能力增强与 caspase-3 和 E-钙黏蛋白下调以及存活素和 CD44 上调有关。

结论

我们的数据表明 ACS5 可促进 CRC 细胞的生长和侵袭,为 CRC 的基因治疗提供了一个潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e8b/5541798/5bb5ebbf9655/CJGH2017-7615736.001.jpg

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