Glycosylation is a common post-translational modification process of proteins. Mucin-type O-glycosylation is an O-glycosylation that starts from protein serine/threonine residues. Normally, it is involved in the normal development and differentiation of cells and tissues, abnormal glycosylation can lead to a variety of diseases, especially cancer. This paper reviews the normal biosynthesis of mucin-type O-glycans and their role in the maintenance of body health, followed by the mechanisms of abnormal mucin-type O-glycosylation in the development of diseases, especially tumors, including the effects of Tn, STn, T antigen, and different glycosyltransferases, with special emphasis on their role in the development of gastric cancer. Finally, tumor immunotherapy targeting mucin-type O-glycans was discussed.

Background Abnormal biogenesis and ribosome free function of ribosomal proteins (RPs) is important for tumorgenesis and development. Ribosomal protein L11 (RPL11) is a component of ribosomal 60 S large subunit with different roles in different cancers. Here, we aimed to unravel the role of RPL11 in non-small cell lung cancer (NSCLC), especially those affecting cell proliferation. Methods RPL11 expression in NCI-H1650, NCI-H1299, A549 and HCC827 and normal lung bronchial epithelial cells HBE was detected using western blotting. The function of RPL11 in NSCLC cells were determined by investigating cell viablity, colony formation and cell migration. Mechanism expoloration of RPL11 effect on NSCLC cells proliferation was explored using flow cytometry, and the effect on autophagy was investigated by the additon of autophagy inhibitor chloroquine (CQ) and endoplasmic reticulum stress (ERS) inhibitor tauroursodeoxycholic acid (TUDCA). Results RPL11 was highly expressed in NSCLC cells. Extopic expression of RPL11 promoted NCI-H1299 and A549 cells proliferation, and migration, and promoted the transition from the G1 phase to the S phase of the cell cycle. Small RNA interference of RPL11 (siRNA) suppressed NCI-H1299 and A549 cells proliferation and migration and arrested the cell cycle in G0/G1 phase. Moreover, RPL11 promoted NSCLC cell proliferation by modulating autophagy and ERS. Expression levels of autophagy and ERS markers were induced by RPL11 overexpression and inhibited by siRPL11. CQ partially suppressed RPL11-induced A549 and NCI-H1299 proliferation: CQ addition reduced RPL11-induced cells viability and clone numbers and reversed the cell cycle process. ERS inhibitor (TUDCA) partially reversed RPL11-induced autophagy. Conclusion Taken together, RPL11 has a tumor-promoting role in NSCLC. It promotes the cell proliferation of NSCLC cells by regulating ERS and autophagy.

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.