Fig 1: RBM38 affects ADM resistance in BC by moderating the expression levels of proteins related to apoptosis, drug resistance and the cell cycle. (A) Western blotting demonstrated that the RBM38/miR-320b signaling axis regulated BC cell biological processes by altering the expression levels of PI3K/AKT signaling pathway-, cell cycle- and drug resistance-related proteins. The quantification of (B) MDR1, (C) BCRP, (D) Bax, (E) Bcl-2, (F) p-PI3K/PI3K and (G) p-AKT/AKT. **P<0.01 and ***P<0.001 as indicated. BM38, RNA binding motif protein 38; miR, microRNA; si, small interfering RNA; MDR1, multiple drug resistant protein 1; BCRP, breast cancer resistance protein; p-, phosphorylated.
Fig 2: Expression levels of RBM38 in BC tissues and cells. (A) RBM38 expression was upregulated in ADM-resistant compared with ADM-sensitive BC tissues. (B) RBM38 expression was upregulated in MCF-7/A cells compared with MCF-7/S cells. (C) mRNA and (D) protein expression levels of RBM38 in MCF-7/S and MCF-7/A cells. **P<0.01 and ***P<0.001. RBM38, RNA binding motif protein 38; BC, breast cancer; ADM, Adriamycin; S, ADM-sensitive cells; A, ADM-resistant cells.
Fig 3: miR-320b promotes the resistance of BC cells to ADM. miR-320b expression levels were downregulated in (A) ADM-resistant BC tissues and (B) MCF-7/A cells compared with ADM-sensitive BC tissues and MCF-7/S cells, respectively. (C) Western blotting demonstrated that RBM38 expression was downregulated in the miR-320b mimics group. (D) miR-320b-inhibited MCF-7/A cells were less susceptible to ADM, and overexpression of miR-320b decreased the IC50 value of ADM. (E) Transwell assays indicated that miR-320b inhibited the invasive ability of ADM-resistant BC cells, magnification, ×100. (F) Cell cycle distribution and (G) apoptosis were analyzed via flow cytometry. *P<0.05, **P<0.01 and ***P<0.001 vs. inhibitor NC, or as indicated; ##P<0.01 and ###P<0.001 vs. mimic NC. miR, microRNA; BC, breast cancer; ADM, Adriamycin; S, ADM-sensitive cells; A, ADM-resistant cells; RBM38, RNA binding motif protein 38; NC, negative control.
Fig 4: RBM38 reverses the effects of miR-320b. (A) mRNA and (B) protein expression levels of RBM38 in MCF-7/A cells were determined using reverse transcription-quantitative PCR and western blotting, respectively. (C) Transwell assays were used to determine invasive ability across different groups, magnification, ×100. (D) Apoptosis and (E) cell cycle distribution were analyzed using flow cytometry. *P<0.05, **P<0.01 and ***P<0.001 as indicated. RBM38, RNA binding motif protein 38; miR, microRNA; ADM, Adriamycin; A, ADM-resistant cells; si, small interfering RNA.
Fig 5: RBM38 impairs the sensitivity of BC cells to ADM, and inhibits the invasive ability of ADM-resistant BC cells. (A) mRNA and (B) protein expression levels of RBM38 in MCF-7/A cells. (C) MCF-7/A cells overexpressing RBM38 were less susceptible to ADM treatment. Furthermore, knockdown of RBM38 decreased the IC50 value of ADM. (D) Invasive ability of si-RBM38-transfected MCF-7/A cells, magnification, ×100. (E) Cell cycle distribution and (F) apoptosis analyses were performed using flow cytometry. **P<0.01 and ***P<0.001 vs. si-NC; #P<0.05, ##P<0.01 and ###P<0.001 vs. pcDNA3.1. RBM38, RNA binding motif protein 38; BC, breast cancer; ADM, Adriamycin; A, ADM-resistant cells; si, small interfering RNA; NC, negative control.
Supplier Page from Abcam for Anti-RBM38 antibody - C-terminal