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. 2022 Sep 6;48(4):181. doi: 10.3892/or.2022.8396

Figure 5.

Figure 5.

Knockdown of ClC-3 expression in A549 cells prevents PTX resistance induced by upregulation of SOX2 expression. (A) (Left) Protein expression levels of MDR1, ABCC2, ABCC10 and tubulin in A549 cells transfected with ClC-3 plasmid or siSOX2 and its control vector or siNC. (Right) Protein expression was semi-quantified using ImageJ. (B) Viability was examined using a CCK-8 assay in A549 cells transfected with ClC-3 plasmid or siSOX2 and its control vector or siNC. Cells were treated with PTX for 48 h. (C) (Left) Protein expression levels of MDR1, ABCC2, ABCC10 and tubulin in A549 cells transfected with SOX2 plasmid or siClC-3 and its control vector or siNC. (Right) Protein expression was semi-quantified using ImageJ. (D) Viability was examined using a CCK-8 assay in A549 cells transfected with SOX2 plasmid or siClC-3 and its control vector or siNC. Cells were treated with PTX for 48 h. Tubulin were used as a loading control in western blotting. All data are presented as the mean ± standard deviation. **P<0.005, ***P<0.001. ns, not significant. Relative, vs. respective control. ClC-3, chloride voltage-gated channel 3; A549-PTX cells, paclitaxel-resistant A549 non-small cell lung cancer cells; PTX, paclitaxel; MDR1, multidrug resistance mutation 1; ABCC2, ATP binding cassette subfamily C member 2; ABCC10, ATP binding cassette subfamily C member 10; siRNA/si, small interfering RNA; CCK-8, Cell Counting Kit-8.