Pseudouridylate Synthase 7 Promotes Cell Proliferation and Invasion in Colon Cancer Through Activating PI3K/AKT/mTOR Signaling Pathway

Background Colorectal cancer is commonly malignant tumor. Herein, we demonstrate that pseudouridylate synthase 7 (PUS7) is closely related to colon cancer. But the biological role of PUS7 in colon cancer is not known. Aims The present study aims to investigate the effects of PUS7 in colon cancer clinical samples and cells and the related molecular mechanism. Methods A profile data set was downloaded from the Cancer Genome Atlas database, which included data from colon cancer tissue samples and normal tissue samples. The top 200 differentially expressed genes were subsequently investigated by a protein-protein interaction (PPI) network. RT-PCR and western blot assays were used to determine gene expression levels. CCK8 assay, colony formation experiment, transwell and flow cytometry assay were used to determine cell viability, proliferation, invasion, and apoptosis, respectively. Results PUS7 is a key gene from the most significant module of the PPI network. PUS7 was upregulated in colon cancer tissues and cell lines. Moreover, PUS7 overexpression is significantly related to the poor survival rate for 60 colon cancer's patients. Cell proliferation and invasion was significantly reduced by PUS7 inhibition and promoted by PUS7 overexpression. The protein levels of cleaved caspase-3/9, c-myc, E-cadherin and vimentin genes were significantly regulated in colon cancer cells transfected with PUS7 interference or overexpression. PUS7 overexpression significantly upregulated the phosphorylation levels of PI3K, AKT and mTOR. Conclusion The results of this study demonstrate that PUS7 overexpression upregulates cell proliferation, invasion and inhibits cell apoptosis of colon cancer cells via activating PI3K/AKT/mTOR signaling pathway.