Fig 1: Down-regulatory effects of SLC7A11 on P-gp expression in MCF-7S cells. (A) SLC7A11 mRNA and protein levels were efficiently reduced by siRNA. (B) SLC7A11-siRNA increased P-gp mRNA expression, in a negatively dependent way. (C) SLC7A11 silence stimulated P-gp expression, shown by immunofluorescence analysis, with flow cytometry. (D) SLC7A11 silence increased the intracellular ROS level and P-gp mRNA expression, which could be reversed by NAC (10 mM, 24 h). (E) SLC7A11 silence enhanced P-gp protein expression, which could be reversed by NAC (10 mM, 24 h), as shown with laser confocal scanning analysis. Scale bar: 20 µm. (F) SLC7A11 silencing enhanced the function of P-gp, which could be reversed by NAC (10 mM, 24 h), and Rho 123 was identified as a typical substrate of P-gp. Scale bar: 100 µm. (G) Treatment with an SLC7A11 inhibitor, sulfasalazine, increased ROS levels and P-gp mRNA expression. All of the experiments were conducted in triplicate, and data with error bars are presented as the mean ± SD (n = 3). *p < 0.05; **p < 0.01 vs. control.
Fig 2: Effect of SLC7A11 over-expression on P-gp expression in MCF-7S and MCF-7R cells. (A) SLC7A11 over-expression reduced the ROS level in MCF-7S and MCF-7R cells. (B) SLC7A11 over-expression inhibited P-gp mRNA expression in MCF-7S and MCF-7R cells. Furthermore, MCF-7S cells that over-expressed SLC7A11 were more sensitive to ADR, compared to MCF-7S cells that has been exposed to a control vector. (C) SLC7A11 over-expression increased the cytotoxic sensitivity of ADR on MCF-7S cells. (D) SLC7A11 over-expression reduced ROS levels and P-gp mRNA expression in MCF-7S cells, which could be reversed by H2O2. (E) SLC7A11 over-expression decreased the function of P-gp, which could be reversed by H2O2 (0.25 mM, 24 h), as indicated by intracellular Rho 123 accumulation in MCF-7S cells. Scale bar: 100 µm. All of the experiments were conducted in triplicate, and data with error bars are presented as the mean ± SD (n = 3). *p < 0.05; **p < 0.01 vs. control.
Fig 3: SNHG6 regulated the sensitivity of PTX-resistant PCa cells to PTX by miR-186. a–e The si-NC, si-SNHG6, si-SNHG6 + anti-NC, or si-SNHG6 + anti-miR-186 was transfected into PC-3/R and DU145/R cells. a, b MTT assay was used to analyze the IC50 value of PC-3/R and DU145/R cells. c The apoptotic rate of PC-3/R and DU145/R under PTX (30 nM) treatment was detected through flow cytometry assay. d, e The levels of cleaved casp-3, cleaved casp-9, MRP1, and MDR1 in PC-3/R and DU145/R cells under PTX (30 nM) treatment was evaluated with western blot analysis. *P < 0.05, **P < 0.001 and ***P < 0.001
Fig 4: The MDR1 mRNA expression levels in tumor cells of leukemia patients. The following scale was used for the distribution of patients with acute myeloid leukemia (A), acute lymphoblastic leukemia (B), and chronic lymphocytic leukemia (C) in accordance with MDR1 mRNA expression levels in tumor cells: weak expression corresponds to 0–15% of the level of KB-8-5 cells, moderate expression corresponds to 15–25% of the level of KB-8-5 cells, and strong expression corresponds to >25% of the level of KB-8-5 cells.
Fig 5: Correlations between the therapy response, cell sensitivity to chemotherapeutic drugs, MDR1 mRNA and P-glycoprotein expression, immunological markers, and cytogenetic abnormalities in leukemia patients. Correlation coefficients reflecting the statistical relationships between the studied parameters were evaluated for patients with acute myeloid leukemia (A), acute lymphoblastic leukemia (B), chronic lymphocytic leukemia and chronic myeloid leukemia (C). Red arrows indicate strong positive correlations (0.70 = rs = 1.00), blue arrows indicate moderate positive correlations (0.30 =rs = 0.69), green arrows indicate weak positive correlations (0.01 = rs = 0.29), and gray arrows indicate no correlations.
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