MicroRNA‑16/VEGFR2/p38/NF‑κB signaling pathway regulates cell growth of human pituitary neoplasms.

Abstract

The association of microRNA (miRNA) with tumor has gradually become an active medical research field, since its discovery in 1993. The aim of the present study was to clarify how microRNA‑16 expression affects the proliferation and survival of pituitary tumor, revealing its potential mechanism. MicroRNA‑16 expression of pituitary tumor patients was observably declined, compared with the normal group. A high expression of microRNA‑16showed longer survival in pituitary tumor patients, compared to a low expression of microRNA‑16 in pituitary tumor patients. MicroRNA‑16 upregulation effectively decreased cell proliferation and induced apoptosis in HP75 cells. MicroRNA‑16 overexpression effectively induced p27, Bax protein expression and caspase‑3/8 activities, and suppressed phosphorylation-(p)-p38, NF‑κB, MMP‑9 and VEGFR2 protein expression in HP75 cells. After VEGFR2 suppression, the effects of microRNA‑16 overexpression on cell proliferation and apoptosis were significantly inhibited in HP75 cells. Moreover, the effects of microRNA‑16 overexpression on p27, Bax protein expression and caspase‑3/8 activities were significantly decreased in HP75 cells after p38 suppression. VEGFR2 or NF‑κB suppression reduced the effects of microRNA‑16 overexpression on p‑p38, NF‑κB, MMP‑9 and VEGFR2 protein expression inhibition in HP75 cells. Our results suggest that microRNA‑16 expression affects the proliferation and angiogenesis of pituitary cancer through the VEGFR2/p38/NF‑κB signaling pathway.