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.

Highlights

  • Gastric carcinoma (GC) is one of the most common malignancies in the world [1,2,3]

  • There was a marked correlation between the levels of miR-152 and B7 homolog 1 (B7-H1) mRNA in gastric cancer tissues

  • Recent studies have focused on immunotherapies by targeting B7 homolog 1 (B7-H1) or programmed death 1 (PD-1) in multiple cancers treatment [4, 5]

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Summary

Introduction

Gastric carcinoma (GC) is one of the most common malignancies in the world [1,2,3]. Despite improvements in diagnosis and treatments was developed in recent years, the advanced gastric cancer is still one of the most lethal cancers due to lack of effective therapies. MiR-152 directly bind to B7-H1 3′ untranslated region in gastric cancer cell and inhibited B7-H1 expression. MiR-152 was reported down regulated in gastric cancer tissues compared to matched normal tissues and low expression of miR-152 was correlated with increased tumor sizes and stage [23]. Expression of miR-152 was decreased in gastric cancer tissues and cell lines compared to non-tumor control

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