Fig. 5

CAFs transactivated HOTAIR expression to induce EMT by targeting CDK5 signaling. a Western blotting indicated that CDK5 expression was significantly increased in recombinant TGF-β1- or CAF-CM treated cells, whereas the EGR-1 and CDK5RAP1 expression levels were greatly decreased. b The histone methylation status of CDK5 signaling was determined with a CHIP assay, which indicated that H3K27me3 was enriched at the promoter of EGR-1 and CDK5RAP1 in CAF-CM-treated MDA-MB-231 and MCF-7 cells, whereas the depletion of HOTAIR blocked this function of CAFs. The results are presented as the fold-change over the control. c ChIP analysis revealed that elevated EZH2 was recruited to the EGR-1 and CDK5RAP1 promoter in MDA-MB-231 and MCF-7 cells. All experiments were repeated three times. *P < 0.05 vs. negative control