RPL11 promotes non-small cell lung cancer cell proliferation via regulating endoplasmic reticulum stress and cell autophagy

Abstract

Background Abnormal ribosomal proteins (RPs) biogenesis and function works importantly in tumorigenesis and development. RPL11 is a component of ribosomal 60S large subunit has different roles in different cancers. Here, we aims to unravel the novel functions of RPL11 in non-small cell lung cancer (NSCLC), especially that affecting cell proliferation. Methods Expression level of RPL11 in different NSCLC cell lines was detected using western blotting. The function of RPL11 in NSCLC cells were CCK-8, colony formation and scratch wound healing detected. Mechanisms of RPL11 on NSCLC cells proliferation were explored by flow cytometry, autophagy detection, and usage of an autophagy inhibitor chloroquine (CQ) and ERS inhibitor (TUDCA) . Results We found that RPL11 was highly expressed in NSCLC cells. Additionally, RPL11 overexpression promoted NSCLC cells proliferation and migration in vitro, and promoted the transition from G1 phase to S phase of the cell cycle. Conversely, RPL11 inhibition suppressed NSCLC cell proliferation and migration, and arrested the cell cycle in G0/G1 phase. Moreover, RPL11 promotes NSCLC cell proliferation via modulating autophagy and ERS. Expression levels of autophagy and ERS markers were induced by RPL11 overexpression, and inhibited by siRPL11. Usage of an autophagy inhibitor chloroquine (CQ) partially reverse the promotion of RPL11 on NSCLC cells proliferation. Besides, RPL11 induced autophagy markers expression could partially reversed by the ERS inhibitor (TUDCA). Conclusions Taken together, RPL11 has a tumor-promoting role in non-small cell lung cancer. It promote the cell proliferation of NSCLC cells by regulating ERS and autophagy.