fig2

Role of cellular reprogramming and epigenetic dysregulation in acquired chemoresistance in breast cancer

Figure 2. Epigenetic deregulation mediates cellular reprogramming in acquired chemoresistance in breast cancer. Upon exposure to chemotherapy, cancer cells which develop transient (drug tolerant phenotype) may further acquire cancer stem cell (CSC)-like features characterized by enrichment for stem cell markers, slow-cycling and quiescence to facilitate higher levels of resistance development. Similarly, cancer cells preferentially evoke EMT process to evade cytotoxicity. During EMT process, cells with epithelial phenotype progressively loose epithelial markers and gain mesenchymal markers to become aggressive and invasive phenotype. EMT and CSC cross-talk using same signaling pathways to establish acquired resistance. Epigenetic deregulation mediates the acquisition of both EMT and stemness to induce chemoresistance, thus, potential epigenetic therapy targeting the cellular reprogramming could address chemoresistance issues

Cancer Drug Resistance
ISSN 2578-532X (Online)

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