HSP90/c-Myc Axis regulated by lncRNA LINC00461 upregulation inhibited the ubiquitination of c-Myc and promotes glucose Metabolism and proliferation through LDHA in Triple-negative Breast Cancer

Abstract LINC00461 represents a new long noncoding RNA. However, it is unclear whether LINC00461 is associated with glucose metabolism and proliferation in triple-negative breast cancer. Here, we show that LINC00461 overexpression induces glucose metabolism and proliferation in TNBC, whereas its downregulation markedly reduces glucose metabolism and proliferation. Mechanistically, LINC00461 might function in TNBC by binding with HSP90. Then, it enhances the interaction between HSP90 and c-Myc and inhibits ubiquitination and degradation of c-Myc to regulate c-Myc target genes-LDHA. Clinically, LINC00461 has tight associations with tumor grade and TNM in cancer patients. There is compelling evidence LINC00461 may be exploited as a possible novel molecular marker and therapeutic target in TNBC.