MicroRNA-128 increases glioma cell radio-sensitivity by suppressing senescent evasion through oncogene Bmi-1.

Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. Classical treatment of glioblastoma includes surgical resection followed by radiation and chemotherapy. However, radio-resistance is always a challenge for the treatment. MicroRNA-128 was found at lower expression in glioma tissues compared to normal tissue. Its downstream target gene, Bmi-1, was associated with self-renewal and differentiation of neural stem cells and could promote the growth of glioma. Our previous studies showed that expression of Bmi-1 can increase following exposure to X-ray radiation, implying that Bmi-1 may confer radio-resistance to glioma. However, the mechanism is still unclear. In this study, we found that overexpression microRNA 128 could inhibit growth of glioma cells and expression of Bmi-1 (P<0.05). Following exposure the 8 Gy X-ray, the growth of cells was inhibited in the microRNA-128 overexpression group compared to the control group (P<0.05). Expression of Bmi-1 was also lower (P<0.05) and the ratio of senescent cells was higher (P<0.05) in the microRNA-128 overexpression group than the control group. Thus, our results suggest that overexpression of micro-RNA128 could increase the radio-sensitivity of glioma cells through Bmi-1. This mechanism may inhibit senescent evasion in glioma cells and provides a novel view for how to resolve the radio-resistance of glioma and investigate a new strategy for glioma radiation treatment regimens.