miR-146a regulates the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF-κB signaling by targeting TRAF6

The aim of the present study was to investigate whether miRNA-146a regulated the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis. miR-146a expression was increased in human cervical cancer. Both overall survival (OS) and disease-free survival (DFS) of low miR-146a expression were higher than those of high miR-146a expression. Additionally, IL-17a expression was lower in patients with high miR-146a expression compared to that of patients with lower miR-146a expression. In a co-culture of cervical cancer and CD4(+) T cells, downregulation of miR-146a inhibited cell growth and induced apoptosis of cervical cancer cells, while overexpression of miR-146a promoted cell growth and reduced apoptosis of cervical cancer cells. Downregulation of miR-146a induced TRAF6 and NF-kappa B protein expression, increased IL-6, IL-17A and IL-21 levels, and enhanced p-STAT3 protein expression. The inhibition of TRAF6 attenuated the effects of anti-miR-146a on the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis. Collectively, miR-146a regulated the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF-kappa B signaling by targeting TRAF6. miR-146a may function as an oncogene in cervical cancer via Th17 cell differentiation by targeting TRAF6.