Research Paper Volume 13, Issue 21 pp 24171—24191

LncRNA OTUD6B-AS1 promotes paclitaxel resistance in triple negative breast cancer by regulation of miR-26a-5p/MTDH pathway-mediated autophagy and genomic instability

The effects of miR-26a-5p/MTDH pathway on regulation of PTX resistance. (A) The relative cell viability of HCC1937 cells, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48 h-treatment of PTX, detected by CCK8 assay. (B) The absorbance of different generations of PTX-resistance HCC1937 is treated with 48 h-treatment of paclitaxel, detected by CCK8 assay. (C) Clone formation of HCC1937, which are treated with different treatments. (D) The proliferation of HCC1937, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48 h-treatment of PTX, detected by Edu assay. (E) The cellular viability of HCC1937, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48h-treatment of PTX detected by Alive/Dead assay. (F) The proliferation of HCC1937, which are treated with liposome, si-MTDH, or ov-MTDH (MTDH re-combination plasmid) for 24 h followed by 48 h-treatment of PTX, detected by Edu assay; (G) The cellular viability of HCC1937, which are treated with liposome, si-MTDH, or ov-MTDH for 24 h followed by 48 h-treatment of PTX detected by Alive/Dead assay. (H and I) Subcutaneously transplantation tumor model.

Figure 6. The effects of miR-26a-5p/MTDH pathway on regulation of PTX resistance. (A) The relative cell viability of HCC1937 cells, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48 h-treatment of PTX, detected by CCK8 assay. (B) The absorbance of different generations of PTX-resistance HCC1937 is treated with 48 h-treatment of paclitaxel, detected by CCK8 assay. (C) Clone formation of HCC1937, which are treated with different treatments. (D) The proliferation of HCC1937, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48 h-treatment of PTX, detected by Edu assay. (E) The cellular viability of HCC1937, which are treated with miR-mimic, miR-inhibitor, or miR-con for 24 h followed by 48h-treatment of PTX detected by Alive/Dead assay. (F) The proliferation of HCC1937, which are treated with liposome, si-MTDH, or ov-MTDH (MTDH re-combination plasmid) for 24 h followed by 48 h-treatment of PTX, detected by Edu assay; (G) The cellular viability of HCC1937, which are treated with liposome, si-MTDH, or ov-MTDH for 24 h followed by 48 h-treatment of PTX detected by Alive/Dead assay. (H and I) Subcutaneously transplantation tumor model.