Silencing RPL8 inhibits the progression of hepatocellular carcinoma by down-regulating the mTORC1 signalling pathway

This study aimed to explore the role of ribosomal protein L8 (RPL8) in controlling hepatocellular carcinoma (LIHC) development. We measured RPL8 expression, apoptosis, cell viability, proliferation, migration, invasion, glucose uptake, lactate production, and the ATP/ADP ratio of LIHC cells to investigate the effect of RPL8 on LIHC. Bioinformatic analysis was employed to analyse RPL8 expression and its potential mechanism in LIHC. RPL8 was upregulated in LIHC tissues and cells. RPL8 silencing accelerated apoptosis and suppressed viability, growth, and movement of LIHC cells. Additionally, RPL8 silencing inhibited glycolysis in LIHC cells. Bioinformatic analysis revealed that RPL8 is regulated by the upstream transcription factor upstream stimulating factor 1 (USF1) and activates the mTORC1 signalling pathway. USF1 overexpression eliminated the inhibitory effect of RPL8 silencing in LIHC cells. RPL8 overexpression increased cell growth, movement, and glycolysis in LIHC. However, inhibition of the mTORC1 signalling pathway eliminated the effect of RPL8 overexpression on LIHC cells. In conclusion, RPL8 may affect LIHC progression by regulating the mTORC1 signalling pathway.