Abstract
MYC is a notorious oncogene in a vast network of malignancies, whereas liver-specific microRNA- (miR-) 122-5p is downregulated in hepatocellular cancer (HCC). Here, we studied the possible correlation between these two and their involvement in glycolysis in HCC. MYC was overexpressed in HCC tissues and cells compared to normal liver tissues and normal hepatocytes NHC, which predicted a poor survival of HCC sufferers. Functional assays demonstrated that silencing of MYC inhibited the glycolysis in HCC cells, as evidenced by significantly weaker glucose consumption, lactate production, adenosine triphosphate (ATP) levels, and downregulated HK1 and HK2 protein expression. Moreover, MYC bound to the miR-122-5p promoter and repressed the miR-122-5p expression. Rescue experiments showed that miR-122-5p inhibitor rescued the diminished glycolysis after MYC silencing. In addition, lactate dehydrogenase (LDHA) was identified as a downstream target of miR-122-5p. The overexpression of LDHA mitigated the effects of si-MYC and miR-122-5p mimic on glycolysis of HCC cells, respectively. In conclusion, the MYC/miR-122-5p/LDHA axis modulates glycolysis in HCC cells and possibly affects HCC progression.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
