Oncotarget

Research Papers:

RASSF1A inhibits gastric cancer cell proliferation by miR-711- mediated downregulation of CDK4 expression

Aijun Liao _, Gao Tan, Lin Chen, Weiwei Zhou and Hongsai Hu

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Oncotarget. 2016; 7:5842-5851. https://doi.org/10.18632/oncotarget.6813

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Abstract

Aijun Liao1,2,*, Gao Tan3,*, Lin Chen1, Weiwei Zhou1, Hongsai Hu1

1Department of Gastroenterology, The First Affiliated Hospital of South China University, Hengyang, Hunan Province, China

2Gastric Cancer Research Center of Hunan Province, Hunan, China

3Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China

*These authors have contributed equally to this work

Correspondence to:

Gao Tan, e-mail: [email protected]

Aijun Liao, e-mail: [email protected]

Keywords: RASSF1A, miR-711, CDK4, gastric cancer, cell cycle

Received: August 27, 2015    Accepted: December 05, 2015    Published: January 02, 2016

ABSTRACT

Although interaction with DNA repair proteins has demonstrated that RASSF1A is a tumour suppressor gene, much attention has been directed in recent years towards its roles in regulating the cell cycle. However, the precise mechanism remains unclear. Uncovering how RASSF1A participates in regulating the cell cycle is critical to exploring effective therapeutic targets for gastric cancer. Here we show that RASSF1A could regulate 14 miRNAs’ expression in the typical human gastric cancer line SGC-7901, of which miR-711 was upregulated the most. Moreover, for SGC-7901 cells, miR-711 was found to downregulate CDK4 expression, and to arrest the cell cycle in the G1 phase. Our results suggest that RASSF1A inhibits the proliferation of gastric cancer cells by upregulating the expression of miR-711, which arrested gastric cancer cells in the G1 phase by downregulating expression of CDK4. This finding might provide us with a novel therapeutic target for gastric cancer by increasing RASSF1A expression via miR-711 regulation.


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