Fig 2: Model showing how miR-383 defects induce the expression of RBM24 to mediate chemotherapy resistance in lung adenocarcinoma cells. RBM24, RNA binding motif protein 24; miR, microRNA; p-, phosphorylated; NF-κB, nuclear factor κB; IκBα, inhibitor α of NF-κB; Bcl-2, B-cell lymphoma-2; Bcl-xL, B-cell lymphoma-xL.

Fig 3: RBM24 upregulation in cancer cells is associated with a worse prognosis in patients with lung cancer. (A) Representative images showing strong, moderate and weak staining of RBM24 in lung cancer tissues and their corresponding non-cancerous lung tissues using an immunohistochemistry tissue array. Magnification, ×100; scale bar, 100 μm. (B and C) Pie charts showing the percentage of (B) lung cancer samples classed as showing strong, moderate or weak RBM24 expression and (C) the corresponding non-cancerous lung tissues. (D) Kaplan-Meier analysis of overall survival in patients with lung cancer based on the expression of RBM24 protein in lung cancer tissues; P=0.0061. RBM24, RNA binding motif protein 24; Cum, cumulative.

Fig 4: miR-383 enhances the cisplatin sensitivity of lung adenocarcinoma cells in vivo. (A) Tumor sizes of the Le-control and Le-miR-383 groups after 3 weeks of treatment with cisplatin. n=9. (B) Average rate of reduction of tumor volume in the indicated groups. *P<0.05. (C) Scatter plot showing the weight of tumors and horizontal lines indicate the average values. *P<0.01. (D) Representative images showing immunohistochemical staining analysis of the expression of the indicated genes. Magnification, ×100; scale bar, 50 μm. miR, microRNA; A549/CDDP, cisplatin-resistant A549 cells; Le, lentiviral vector; p-, phosphorylated; RBM24, RNA binding motif protein 24.

Fig 5: miR-383 enhances the sensitivity of lung adenocarcinoma cells to cisplatin through negative regulation of RBM24. (A) Protein expression levels of RBM24 were determined by immunoblotting in A549/CDDP and parental A549 cells. (B) A549/CDDP cells were transfected with siRNA NC or RBMA24 siRNA for 48 h, and RBM24 expression as assessed using western blotting. (C) Effect of RBM24 knockdown on the viability of A549/CDDP cells after treatment with different concentrations of cisplatin for 48 h. (D) Western blotting was used to determine the expression of RBM24 in A549 cells stably overexpressing RBM24 cells; uninfected and control lentivirus-infected A549 cells served as controls. (E) Effect of stable overexpression of RBM24 on the viability of A549 cells after treatment with different concentrations of cisplatin for 48 h. (F) A549 cells were transfected with miRNA NC or miR-383 inhibitor for 48 h, and RBM24 expression was assessed using western blotting. (G) Effect of miR-383 knockdown on the viability of A549 cells after treatment with different concentrations of cisplatin for 48 h. (H) A549 cells were co-transfected with miR-383 inhibitor and either RBM24 siRNA or siRNA NC for 48 h, and RBM24 expression was assessed by western blotting. (I) Effect of miR-383 and RBM24 knockdown on the viability of A549 cells after treatment with different concentrations of cisplatin for 48 h. (J) Representative images showing detectable comet tails visualized under a fluorescence microscope. Magnification, ×200; scale bar, 50 µm. Data are presented as the mean ± standard deviation of three independent experiments. *P<0.05. miR, microRNA; RBM24, RNA binding motif protein 24; A549/CDDP, cisplatin-resistant A549 cells; siRNA, small interfering RNA; NC, nonsense control; miR/miRNA, microRNA.