Oncotarget

Research Papers:

miR-135a inhibits tumor metastasis and angiogenesis by targeting FAK pathway

Zhenguo Cheng, Funan Liu, Hongyan Zhang, Xiaodong Li, Yanshu Li, Jiabin Li, Furong Liu, Yu Cao, Liu Cao and Feng Li _

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Oncotarget. 2017; 8:31153-31168. https://doi.org/10.18632/oncotarget.16098

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Abstract

Zhenguo Cheng1, Funan Liu2, Hongyan Zhang1, Xiaodong Li1, Yanshu Li1, Jiabin Li1, Furong Liu1, Yu Cao1, Liu Cao1, Feng Li1

1Department of Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China

2Department of Surgical Oncology, The first Hospital of China Medical University, Shenyang 110001, China

Correspondence to:

Feng Li, email: fli@mail.cmu.edu.cn

Keywords: gastric cancer, metastasis, miR-135a, FAK, p53

Received: September 27, 2016     Accepted: March 01, 2017     Published: March 10, 2017

ABSTRACT

Tumor metastasis has been the major cause of recurrence and death in patients with gastric cancer. Here, we find miR-135a has a decreased expression in the metastatic cell lines compared with its parental cell lines by analyzing microRNA array. Further results show that miR-135a is downregulated in the majority of human gastric cancer tissues and cell lines. Decreased expression of miR-135a is associated with TNM stage and poor survival. Besides, regaining miR-135a in gastric cancer cells obviously inhibits tumor growth, migration, invasion and angiogenesis by targeting focal adhesion kinase (FAK) pathway. Bioinformatics analysis and molecular experiments further prove that miR-135a is a novel downstream gene of tumor suppressor p53. Blocking FAK with its inhibitor can also enhance miR-135a expression through inducing p53. In summary, this study reveals the expression and function of miR-135a in gastric cancer and uncovers a novel regulatory mechanism of miR-135a.


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