MicroRNA-195 suppresses rectal cancer growth and metastasis via regulation of the PI3K/AKT signaling pathway

MicroRNAs (miRNAs) play a vital role in the progression of cancer, however, only limited data on miRNAs in rectal cancer are available. The aim of the present study was to investigate whether miR-195 could inhibit the progression of rectal cancer. The miR-195 mimic was transfected into 2 types of human rectal cancer cells (SW837 and SW1463). Cell viability and apoptosis were analyzed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, and cell migration and invasion were assessed by scratch test and Transwell assay. The results revealed that insulin-like growth factor 1 (IGF1) was predicted as a potential target of miR-195 by Targetscan7.2, and the result was verified by dual-luciferase reporter assay. The co-transfection of IGF1 was performed to confirm the underlying mechanism of tumor suppressor of miR-195 in rectal cancer. The activation of PI3K/AKT signaling was determined by western blotting. The levels of miR-195 in SW837 and SW1463 cells were revealed to be lower than in human rectal mucosa epithelial cells. After the transfection with miR-195, the cell viability was decreased, while the apoptosis was significantly increased (SW837: 5.21% vs. 20.96%; SW1463: 4.19% vs. 25.22%). Moreover, cell migration and invasion were significantly inhibited in the mimic group. miR-195 specifically targeted IGF1, however, the co-transfection of IGF1 could partially reverse the inhibitory effects of miR-195 on rectal cancer cells. It was also determined that the phosphorylation of PI3K and AKT were significantly inhibited in the mimic group. The tumor suppressive ability of miR-195 in rectal cancer cell proliferation and metastasis was mediated by blocking IGF1 expression and inhibiting the PI3K/AKT pathway.