Oncotarget

Research Papers:

MicroRNA-152 regulates immune response via targeting B7-H1 in gastric carcinoma

Yaxin Wang, Di Wang, Gengchen Xie, Yuping Yin, Ende Zhao, Kaixiong Tao and Ruidong Li _

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Oncotarget. 2017; 8:28125-28134. https://doi.org/10.18632/oncotarget.15924

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Abstract

Yaxin Wang2, Di Wang1, Gengchen Xie1, Yuping Yin1, Ende Zhao1, Kaixiong Tao1, Ruidong Li1

1Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

2Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

Correspondence to:

Kaixiong Tao, email: tao_kaixiongg@yahoo.com

Ruidong Li, email: liruidonghust@163.com

Keywords: gastric cancer, microRNA-152, B7-H1, immune response

Received: December 19, 2016     Accepted: February 20, 2017     Published: March 06, 2017

ABSTRACT

MiR-152 has been reported may be involved in carcinogenesis in gastric cancer. However, its role has not been comprehensively investigated in gastric cancer. We found miR-152 in human gastric cancer tissues were significantly lower than that in matched adjacent normal tissues. Meanwhile, lower miR-152 was also found in gastric cancer cell lines. The stage, tumor size and lymph node metastasis rate were significant higher in low–miR-152 group in clinical patients. Furthermore, there was a marked correlation between the levels of miR-152 and B7-H1 mRNA in gastric cancer tissues. Mechanistically, miR-152 directly bind to B7-H1 3′ untranslated region in gastric cancer cell and inhibited B7-H1 expression. Functional study demonstrated that elevation of miR-152 enhanced T cells proliferation and effector cytokines production via inhibiting B7-H1/PD-1 pathway. In conclusion, our work identified a novel mechanism by which immune response is increased by expression of miR-152 via targeting B7-H1. MiR-152 may be a potential therapeutic approach for gastric cancer.


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