LncRNA MACC1-AS1/MACC1 enhances the progression of glioma via regulating metabolic plasticity.

This study plans to investigate the effects of long-noncoding RNA MACC1-AS1 on glioma cells and its mechanism at metabolic plasticity angle. The MACC1-AS1 level was identified both in glioma tissues and in cells. Then the effects of MACC1-AS1 abnormal level on cell viability, apoptosis, the expression of apoptosis associated protein, glucose metabolism and redox status were measured in A172 and U251 cells by different methods. Furthermore, the interaction of MACC1-AS1 and MACC1 in glioma cells was investigated and the role of AMPK pathway was specifically examined. Our results demonstrated that MACC1-AS1 level was high in glioma tissues and cells, and MACC1-AS1 overexpression was closely associated with poor prognosis of glioma. Notably, under glucose deprivation, the MACC1-AS1 level was significantly increased, and overexpression of MACC1-AS1 increased cell viability but inhibited apoptosis. Also, MACC1-AS1 overexpression obviously increased the levels of GLUT1, HK2, G6PD, MCT1, ATP, lactate and NAPDH as well as promoted the activities of HK2 and LDHA, while reduced ROS level and the ratio of NADP+/NAPDH. In particular, the effects of proliferation, apoptosis and metabolic plasticity of glioma cells caused by MACC1-AS1 overexpression were achieved by positively regulating MACC1, and MACC1-AS1 promoted MACC1 expression via the AMPK pathway. In conclusions, the MACC1-AS1/MACC1 axis exertes the tumor-promoting effect by regulating glucose metabolism and redox homeostasis in glioma cells by activating the AMPK signals.