C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner

A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to provide a new perspective for regulating glucose metabolism and aerobic glycolysis of BC. In this paper, by downregulating C-myc protein, our team found that the expression of long-chain noncoding RNATSPAR-AS2 was significantly downregulated. However, the expression of long-chain noncoding RNASPAR-AS2 in BC is relatively high, and the prognosis is poor. TSPEAR-AS2 can promote the malignant phenotype of BC cells, including proliferation, apoptosis, invasion and metastasis, and glycolysis. At the same time, TSPEAR-AS2 can also upregulate the expression of GLUT1, an important regulator of glycolysis, thus promoting the metabolic reprogramming of BC. Molecular mechanism experiments show that TSPEAR-AS2 may promote the expression of GLUT1 by participating in IGF2BP2 modified by the GLUT1 gene. Our results suggest that the C-myc/TSPEAR-AS2/GLUT1 axis promotes the invasion and metastasis of BC by inducing glucose metabolism reprogramming. However, more phenotypic and molecular mechanism results need to be further verified.