The reduced DLG5 promotes doxorubicin resistance in breast cancer cells MCF-7 through regulating autophagy.

Breast cancer is among the most prevalent malignant tumors in women globally, with adriamycin (ADM) demonstrating considerable efficacy as a first-line chemotherapeutic agent. The problem of adriamycin resistance significantly impairs its effectiveness, requiring the clarification of resistance mechanisms and the discovery of novel biomarkers to enhance treatment techniques. This research utilizes a blend of cellular studies and data analysis to examine the influence of DLG5 on the expression of autophagy-related genes in doxorubicin-resistant MCF-7 cell lines. The findings imply that autophagy may confer protection to breast cancer cells, whereas the downregulation of DLG5 correlates with adriamycin resistance, indicating its potential as a novel biomarker for predicting treatment responses. Moreover, DLG5 affects the viability of adriamycin-resistant cells by stimulating the autophagy pathway, highlighting its protective function in resistance. This research elucidates the probable pathways by which DLG5 contributes to chemotherapy resistance in breast cancer and underscores its significance as a therapeutic target. This research elucidates the processes of adriamycin resistance, offering valuable insights for the advancement of future breast cancer treatment techniques.