Abstract
Effect of miRNA-200c (miR-200c) on the proliferation, invasion and apoptosis of prostate cancer cell line LNCaP was investigated. The difference in miR-200c expression was observed using RT-qPCR in the NC group (transfected empty plasmid), simulation group (simulation sequence) and inhibition group (transferred inhibition sequence), which were established by transfecting LNCaP cells with a kit. The proliferation, invasion and apoptosis of cells after transfection were detected using the cell counting kit-8 (CCK-8) method, Transwell chamber and flow cytometry. RT-qPCR detection showed that the relative expression of miR-200c in LNCaP cells significantly increased compared with RWPE-1 cells (P<0.05). The difference was statistically significant in the relative expression of miR-200c cells among NC group, simulation group and inhibition group after transfection (P<0.05) and they significantly decreased in NC group of cells compared with the simulation group (P<0.05). CCK-8 detection showed that there were differences at the 2nd, 3rd, 4th and 5th days of growth in the NC group, simulation group and inhibition group of cells (P<0.05) and there was a difference in the proliferation ability between NC group and simulation group (P<0.05). Transwell chamber detection showed that there was a difference in the invasion ability among NC group, simulation group and inhibition group of cells (P<0.05), among which the number of passed membrane cells in inhibition group was significantly smaller than that in NC group and simulation group (P<0.05), and the difference was not statistically significant between NC group and simulation group (P>0.05). Flow cytometry detection of the apoptosis ability of each group of cells showed that there was a difference in the apoptotic rate in the NC, simulation and inhibition groups (P<0.05). The low expression of miR-200c is beneficial to inhibit the proliferation and invasion of LNCaP cells in vitro and to promote apoptosis, which may be a potential target for prostate cancer biotherapy.