Background: Lung adenocarcinoma (LUAD) is a leading cause of mortality associated with cancer globally. Thus, it is essential to elucidate its tumorigenesis and prognosis. Accumulating evidence shows that long noncoding RNAs (lncRNAs) play important roles in the occurrence and progression of tumors by regulating their glucose metabolism.
Methods: Bioinformatics analysis was performed to explore the expression of LINC00551  in LUAD. The level of LINC00551  in LUAD cells and tissues was detected by RT-qPCR. CCK-8, colony formation, EDU and transwell assays were conducted to evaluate the cell growth and migration of LUAD cells (A549 and PC9). High throughput sequencing was used to discover the downstream genes of LINC00551 . The metabolic function of LUAD cells was identified by glucose uptake and lactate production assays. Furthermore, tumor xenografts were established to investigate the effects of LINC00551  on tumor growth in vivo.
Results: Herein, we found that LINC00551  was low-expressed in LUAD, and its level correlated with clinical prognosis. Ectopic expression of LINC00551  inhibited the proliferation and migration of LUAD cells (A549 and PC9). High throughput sequencing and gene enrichment analysis revealed that LINC0551 may be involved in metabolic pathway. Glucose uptake and lactate production assays suggested that LINC00551  suppressed glycolysis of LUAD cells. Mechanistically, our work revealed that LINC00551  inhibited glycolysis in LUAD cells by impairing c-Myc -mediated transcription of an important glycolysis-related enzyme PKM2 .
Conclusion: In summary, our study identifies LINC00551  as a tumor suppressor in LUAD and implicates the LINC00551/c-Myc /PKM2  axis in the glycolytic remodeling of LUAD.
Keywords: lung adenocarcinoma, LINC00551 , c-Myc , PKM2 , glycolysis