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. 2020 Oct 20;11(10):883. doi: 10.1038/s41419-020-03083-8

Fig. 4. miR-372-3p bound by KCNQ1OT1 conferred radiosensitivity in LUAD cells via autophagy inhibition.

Fig. 4

A Scatter plot of differentially expressed miRNAs between KCNQ1OT1 knockdown and control A549/IR cells. B KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis of upregulated miRNAs in KCNQ1OT1-knockdown A549/IR cells, and “regulation of autophagy” was included among the top 10 significant pathways. C qRT-PCR analysis for differentially expressed miRNAs in parental and IR-resistant A549 cells. D Regression analysis for the correlation between KCNQ1OT1 and miR-372-3p in LUAD tumor specimens, n = 50. E Schematic illustration of the potential binding sites of miR-372-3p (middle) and KCNQ1TO1 (KCNQ1OT1-wt, top), and the designed mutant sequence (KCNQ1OT1-mut, bottom). F Luciferase assay in HEK293 cells after cotransfected either KCNQ1OT1-wt or KCNQ1OT1-mut vectors with miR-372-3p mimic. G Western Blot analysis for LC3B-II and p62 protein in miR-372-3p inhibiting A549 and miR-372-3p-expressing A549/IR cells with GAPDH as an endogenous control. H Colony survival assay in miR-372-3p inhibiting A549 and miR-372-3p-expressing A549/IR cells with indicated irradiation dosages. Data are presented as the mean ± SD. from three independent experiments, *p < 0.05.