MiR‐200c inhibits autophagy and enhances radiosensitivity in breast cancer cells by targeting UBQLN1
doi: 10.1002/ijc.29065
pmid: 25044403
MiR‐200c inhibits autophagy and enhances radiosensitivity in breast cancer cells by targeting UBQLN1
Radioresistance is a major challenge during the treatment of breast cancer. A further understanding of the mechanisms of radioresistance could provide strategies to address this challenge. In our study, we compared the expression of miR‐200c in four distinct breast cancer cell lines: two representative basal cancer cells (MDA‐MB‐231 and BT549) vs. two representative luminal cancer cells (MCF‐7 and BT474). The results revealed practically lower expression of miR‐200c in the two basal cancer cell lines and higher expression of miR‐200c in luminal cancer cells compared to the normal breast epithelial cell line MCF‐10A. Ectopic expression of miR‐200c in MDA‐MB‐231 cells inhibited irradiation‐induced autophagy and sensitized the breast cancer cells to irradiation. We also identified UBQLN1 as a direct functional target of miR‐200c involved in irradiation‐induced autophagy and radioresistance. In 35 human breast cancer tissue samples, we detected an inverse correlation between the expression of miR‐200c vs. UBQLN1 and LC3. These results indicate that the identified miR‐200c/UBQLN1‐mediated autophagy pathway may help to elucidate radioresistance in human breast cancer and might represent a therapeutic strategy.
- Nanfang Hospital China (People's Republic of)
- University of California, Los Angeles United States
- Anhui Medical University China (People's Republic of)
- Southern Medical University China (People's Republic of)
- Second Hospital of Anhui Medical University China (People's Republic of)
Epithelial-Mesenchymal Transition, Blotting, Western, Autophagy-Related Proteins, Apoptosis, Breast Neoplasms, Cell Cycle Proteins, Immunoenzyme Techniques, Autophagy, Humans, Breast, Luciferases, Cells, Cultured, In Situ Hybridization, Adaptor Proteins, Signal Transducing, Cell Proliferation, Flow Cytometry, Gene Expression Regulation, Neoplastic, Carcinoma, Basal Cell, Female, Carrier Proteins
Epithelial-Mesenchymal Transition, Blotting, Western, Autophagy-Related Proteins, Apoptosis, Breast Neoplasms, Cell Cycle Proteins, Immunoenzyme Techniques, Autophagy, Humans, Breast, Luciferases, Cells, Cultured, In Situ Hybridization, Adaptor Proteins, Signal Transducing, Cell Proliferation, Flow Cytometry, Gene Expression Regulation, Neoplastic, Carcinoma, Basal Cell, Female, Carrier Proteins
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