MicroRNA-152 regulates immune response via targeting B7-H1 in gastric carcinoma
Metrics: PDF 1218 views | HTML 2333 views | ?
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
Kaixiong Tao, email: email@example.com
Ruidong Li, email: firstname.lastname@example.org
Keywords: gastric cancer, microRNA-152, B7-H1, immune response
Received: December 19, 2016 Accepted: February 20, 2017 Published: March 06, 2017
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.