Long non-coding RNA MIR503HG inhibits the proliferation, migration and invasion of colon cancer cells via miR-107/Par4 axis

Abstract

PurposeColon cancer is a common caner with high death rate in the world. The study aimed to detect the effect and mechanism of long non-coding RNA (LncRNA) MIR503HG on colon cancer. MethodsThe MIR503HG expression was measured in colon cancer tissues and cell lines by qRT-PCR. The proliferation, apoptosis, migration and invasion of colon cancer cells were measured by MTT, flow-cytometry, wound healing and transwell assay. The protein expression of E-cadherin, N-cadherin, and Vimentin was detected by Western blot. The target relationships among MIR503HG, miR-107 and Par4 were predicted by StarBase and TargetScan, and verified by luciferase reporter and RNA pull-down assay. The xenograft tumor model was constructed in mice to verify the inhibitory effect of MIR503HG in vivo. ResultsThe expression of MIR503HG was decreased in colon cancer tissues and cell lines. MIR503HG overexpression inhibited cell proliferation, migration and invasion, promoted cell apoptosis, down-regulated N-cadherin and Vimentin, and up-regulated E-cadherin in colon cancer. MIR503HG negatively regulated its target miR-107. MiR-107 overexpression reversed the anti-tumor effects of MIR503HG overexpression on colon cancer cells. Par4 was a target of miR-107, which was positively regulated by MIR503HG. The promoting effects of MIR503HG silencing on colon cancer cells were eliminated by Par4 overexpression. ConclusionMIR503HG regulated Par4 via sponging miR-107 in colon cancer, which promoting a new idea for the treatment of colon cancer.