miR-137 functions as a tumor suppressor gene in pituitary adenoma by targeting AKT2.

Pituitary adenoma is a common intracranial tumor, but the underlying molecular carcinogenesis mechanisms remain unclear. Accumulative evidence has demonstrated that aberrant expression of microRNAs (miRNAs) is an important feature of cancer. The aim of the current study was to explore the role of miR-137 in pituitary tumor. The expression level of miR-137 in pituitary tumor tissues was measured by quantitative RT-PCR. Then the effects of miR-137 upregulation/downregulation on the proliferation and invasion as well as the potential molecular mechanisms were further investigated. Our results showed that the expression level of miR-137 was significantly reduced in pituitary tumor tissues compared to normal controls. Ectopic expression of miR-137 inhibited the proliferation and invasion of pituitary tumor cells, while miR-137 suppression promoted the proliferation and invasion capacity of cancer cells. Bioinformatic analysis of the downstream targets of miR-137 revealed that many enriched gene ontology functions and pathways were closely associated with carcinogenesis. Mechanically, AKT2 was demonstrated to be a direct downstream target of miR-137. The expression level of miR-137 was negatively correlated with AKT2 in pituitary tumor tissues. Taken together, miR-137 plays a tumor suppressive role in pituitary adenoma through regulating AKT2. IJCEP