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Chemotherapy, radiotherapy, and endocrinotherapy are documented to induce autophagy among breast cancer cells, but the role of autophagy in this disease has been attributed as cytoprotective as well as tumor‐suppressing. Thus we studied  MDA ‐ MB ‐231 and  SK ‐ BR ‐3 breast cancer cell lines treated with epirubicin ( EPI ) to assess autophagy and apoptosis. We found out that  EPI  induced apoptosis and autophagy in both cell lines. The lysosomal inhibitor bafilomycin A1 inhibited cellular autophagy and enhanced  EPI ‐triggered apoptosis, perhaps due to inhibition of autolysosome formation, which then inhibited autophagic effects of engulfing and clearing damaged mitochondria. This inhibition increased mitochondrial cytochrome C release which augmented epirubicin‐induced caspase‐dependent apoptosis and cytotoxicity. In addition, the lysosomal neutralizing agent ammonia chloride ( AC ), and Atg7 knockdown by si RNA , could inhibit epirubicin‐triggered autophagy, enhance cytotoxicity, and increase caspase‐9‐ and caspase‐3‐dependent apoptosis. Thus, autophagy plays a prosurvival role in  EPI ‐treated  MDA ‐ MB ‐231 and  SK ‐ BR ‐3 cells, and autophagy inhibition can potentially reverse this effect and increase the cytotoxicity of  EPI .

Inhibiting autophagy increases epirubicin's cytotoxicity in breast cancer cells