Effect of miR-148a on the radiosensitivity of lung cancer cells

Abstract

Objective To explore the effects of miR-148a on the radiosensitivity of lung cancer cell lines A549, H460, and H1299. Methods Lung cancer cells were divided into various groups based on different treatment methods. (1) A549 and H460 cells were classified into three groups: control, 4 Gy γ-irradiation, and 8 Gy γ-irradiation groups. miR-148a expression levels were analyzed through qRT-PCR. (2) A549 cells were categorized into two groups: control and miR-148a transfection groups. H460 cells were also divided into two groups: control and anti-miR-148a transfection groups. The cells were treated with different doses of γ-irradiation, and cell proliferation was detected through a clonogenic assay. (3) A549 and H1299 cells were grouped into three: control, miR-148a transfection, and miR-148a+ER transfection groups. The cells were treated with different doses of γ-irradiation, and the proliferation of A549 and H1299 cells was detected via clonogenic assay. Statistical significance was determined with SPSS and analyzed with Student t test. P<0.05 was considered statistically significant. Results qRT-PCR analysis revealed that the miR-148a expression in the A549 and H460 cells treated with γ-irradiation decreased significantly. Clonogenic assays showed that miR-148a could sensitize A549 cells exposed to irradiation compared with that of the control group (t=12.16, P<0.01). H460 cells were more resistant to irradiation in the presence of anti-miR-148a (t=11.93, P<0.01). miR-148a overexpression could also downregulate the mRNA and protein levels of estrogen receptor (ER) in A549 cells, but anti-miR-148a could increase the mRNA and protein levels of ER in H460 cells. The miR-148a and ER overexpression significantly decreased the effect of miR-148a on the proliferation of A549 and H1299 cells (t=11.34, 12.68, respectively, both P<0.01). Conclusions Irradiation could decrease miR-148a expression levels, and miR-148a overexpression could downregulate the ER level and suppress the proliferation of A549 and H1299 cells, thereby enhancing the radiosensitivity of lung cancer cells. Key words: Lung neoplasms; Radiation tolerance; MiRNA-148a; Estrogen receptor; Cell proliferation