Abstract
Our study found that MED27 was highly expressed in breast cancer and promoted breast cancer development, especially its metastasis and stemness maintenance, by targeting KLF4 both in vitro and in vivo. Mechanistically, MED27 transcriptionally activated KLF4 by binding to its promoter region in breast cancer cells. MED27 silencing sensitized breast cancer cells to epirubicin therapy. The high expression of MED27 and KLF4 alone or both was positively correlated with the differentiation status of cancer cells and predicted poor prognosis of breast cancer patients. All these findings provide the potential of developing MED27/KLF4 signaling axis as the cascade candidate therapeutic targets and prognosis biomarkers in breast cancer.
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