CRNDE interference inhibits colorectal cancer cell proliferation, migration, and invasion, and promotes apoptosis

The aim of this study was to investigate the effect of colorectal neoplasia differentially expressed ( CRNDE ) interference on the proliferation, migration, invasion, and apoptosis of colorectal cancer (CRC) cells. Lovo, HCT-116, COLO 205, HT-29, SW480, and NCM460 cells were screened by quantitative reverse transcription polymerase chain reaction after transfection with CRNDE -interference vectors or miR-320a mimics. The levels of APPL1, Bax, Bcl-2, and cleaved caspase-3 were determined by western blotting. Cell proliferation was evaluated using Cell Counting Kit-8. Apoptosis was detected using flow cytometry and cell migration and invasion were assessed using a transwell assay. The relationships between CRNDE and miR-320a levels and between APPL1 and miR-320a levels were determined by luciferase reporter assay. The expression levels of CRNDE and APPL1 were significantly higher in HCT-116 cells than in Lovo, COLO 205, HT-29, SW480, or NCM460 cells ( P  < 0.05). miR-320a overexpression and CRNDE interference significantly decreased cell proliferation, migration, and invasion ( P  < 0.05), but significantly increased apoptosis ( P  < 0.05). miR-320a overexpression or CRNDE interference significantly increased the number of cells in the G0-G1 phase, compared to the control treatment and empty vector transfection, while decreasing the number of cells in the G2-M phase. miR-320a overexpression and CRNDE interference significantly increased the expression levels of apoptosis-related proteins ( P  < 0.05). miR-320a inhibited luciferase activity in HCT-116 cells transfected with the wild-type CRNDE 3′-UTR ( P  < 0.05) or the APPL1 3′-UTR ( P  < 0.05). Thus, CRNDE interference inhibited the proliferation, migration, and invasion of CRC cells and promoted apoptosis. The mechanism was related to the CRNDE / miR-320a /APPL1 axis.