EZH2 Confers Sensitivity of Breast Cancer Cells to Taxol by Attenuating p21 Expression Epigenetically

Breast cancer is the leading cause of death in women. Although numerous clinical regimens are used to treat breast cancer and manifest satisfied efficacy, drug resistance is emerging as the major obstacle to their long-term use. It is critically necessary to decipher the molecular mechanism underlying this process to obtain improved and long-term use of each regimen. In the present study, we showed the negative relationship between EZH2 and chemoresistance to taxol in breast cancer cells. EZH2 interference was capable of decreasing while overexpression increasing apoptosis of breast cancer cells challenged with taxol. Meanwhile, p21, the inhibitor of cell cycle entry, interference upregulated, while overexpression downregulated apoptosis induced by taxol. Mechanistically, EZH2 was recruited to the promoter of p21 accompanied with H3K27me3 enrichment and transcription silencing. Collectively, EZH2 attenuates chemoresistance of breast cancer cells to taxol by dampening p21 epigenetically.