Effect of LncRNA UCA1 on radiosensitivity of lung cancer cells and its mechanism

Abstract

Objective To evaluate the effect of long-chain non-coding RNA (LncRNA) UCA1 on the proliferation, apoptosis and radiosensitivity of lung cancer cell and to explore the underlying mechanism. Methods qRT-PCR was used to detect the expression of UCA1 and miR-513a-5p in lung cancer cell A549, H1299 and normal human lung cell HBE. The si-con group (transfected si-con), si-UCA1 group (transfected si-UCA1), miR-513a-5p group (transfected miR-513a-5p mimics), miR-NC group (transfected miR-NC), IR+ si-con group (transfected si-con, and irradiated), IR+ si-UCA1 group (transfected miR-NC and irradiated), IR+ miR-513a-5p group (transfected miR-513a-5p mimics and irradiated), IR+ miR-NC group (transfected miR-NC and irradiated), IR+ si-UCA1+ anti-miR-513a-5p group (co-transfected si-UCA1, anti-miR-513a-5p and irradiated) were transfected into the A549 and H1299 cells by liposome method, and then the cells in certain groups were subject to 4Gy irradiation. The cell proliferation of each group was detected by MTT assay. The sensitivity enhancement ratio was assessed by clone formation assay. The cell apoptosis of each group was detected by flow cytometry. The fluorescence activity of each group was detected by dual-fluorescein gene detection assay. Results Compared with human normal lung cell HBE, the expression levels of UCA1 were significantly up-regulated in the lung cancer cell A549 and H1299(both P<0.05), whereas those of miR-513a-5p were significantly down-regulated (both P<0.05). Inhibition of UCA1 and overexpression of miR-513a-5p significantly inhibited cell proliferation, promoted cell apoptosis and increased the sensitivity of radiation exposure of A549 and H1299(sensitivity enhancement ratio=1.897, 2.146 and 1.615, 1.872). miR-513a-5p could suppress the fluorescence activity of wild-type UCA1 cells, and UCA1 could negatively regulate the expression of miR-513a-5p. Inhibition of miR-513a-5p could reverse the enhancement effect of inhibiting UCA1 upon the radiosensitivity of lung cancer cells. Conclusions Inhibition of LncRNA UCA1 can enhance the sensitivity of radiation exposure to lung cancer cells. The mechanism may be related to the targeted inhibition of miR-513a-5p. Key words: UCA1 gene; miR-513a-5p gene; Radiosensitivity; Lung cancer cell line