microRNAs (miRNAs) are involved in cancer development and progression, and have regulatory roles as tumor suppressors or oncogenes. Although aberrant expression of miR-187 has been observed in several types of cancer, its pathophysiological role and relevance to tumorigenesis in gastric cancer (GC) remains unknown. In the present study, the expression and biological role of miR-187 was investigated in 32 specimens of GC tissues and their adjacent non-tumorigenic controls, and the association between miR-187 expression and clinical features of GC were analyzed further. Kaplan-Meier survival curves determined the clinical significance of miR-187 expression in GC. Following transfection with miR-187 mimics, the biological functions of miR-187 were determined by cell proliferation and cell cycle assays. Moreover, following transfection with miR-187 mimics, the targets regulated by miR-187 were investigated using western blotting. Luciferase reporter assays confirmed whether miR-187 regulated MAD2 mitotic arrest deficient-like 2 (MAD2L2) and stomatin (EPB72)-like 2 (STOML2) expression. The data of the present study revealed that miR-187 was significantly downregulated in GC compared with adjacent non-tumorigenic counterparts. Furthermore, decreased expression of miR-187 correlated with cell differentiation (P<0.05), TNM staging (P<0.05) and poor prognosis in GC patients. Functional studies indicated that miR-187 overexpression evidently inhibited MGC-803 cell proliferation in vitro and altered the cell cycle by arresting cells in the G0/G1 phase. In addition, the luciferase assay and western blotting revealed that MAD2L2 and STOML2 were targeted by miR-187. In conclusion, it is suggested that miR-187 functions as a tumor suppressor in GC, and is important in the development and progression of GC. Moreover, miR-187 may be a potential biomarker and therapeutic target in GC.
Keywords: gastric cancer; miR-187; microRNA; mitotic arrest deficient-like 2; stomatin (EPB72)-like 2.