MiR-216a-5p inhibits tumorigenesis in Pancreatic Cancer by targeting TPT1/mTORC1 and is mediated by LINC01133

摘要

MiR-216a-5p has opposite effects on tumorigenesis and progression in the context of different tumors,acting as either a tumor suppressor or an oncogene. However, the expression and function ofmiR-216a-5p in pancreatic cancer (PC) is not well characterized.In this study, we found miR-216a-5p was significantly downregulated in PC tissues and cell lines, whichshowed a negative correlation with peripancreatic lymph, perineural invasion and TNM stage of PCspatients. We made use of functional assays to reveal that miR-216a-5p inhibited growth and migration ofPC cells in vitro and in vivo. Then, by employing the bioinformatics analysis and luciferase reporter assay,we demonstrated TPT1 was a potential target of miR-216a-5p, which contributes to tumor malignance bymediating mTORC1 pathway-associated autophagy. Furthermore, bioinformatics analysis and RNApulldown confirmed that miR-216a-5p was mediated by LINC01133, which sponge miR-216a-5p, as acompeting endogenous RNA (ceRNA). Collectively, our study revealed an important role ofLINC01133/miR-216a-5p/TPT1 axis in the genesis and progression of PCs, which provides potentialbiomarkers for clinical diagnosis and therapy of PCs.