Fig. 5

The EZH2-Integrin α11 axis regulates EMT in drug-resistant breast cancer cells

(A) Heat map showing the expression of selected EMT-associated genes in TAMR and ADR cells compared to parental MCF-7 cells. (B) Comparison of E-cadherin and Vimentin expression levels in MCF-7, TAMR, and ADR cells stained with fluorescence-labelled antibodies. The scale bar (white) represents 30 μm at an original magnification of 400×. (C, D) Immunoblots demonstrating the effects of overexpression of SUZ12 or EZH2 (C) and silencing of ITGA11, SUZ12, or EZH2 (D) on the expression of epithelial (E-Cadherin, Keratin19) and mesenchymal cell markers (Vimentin, Snail, ZEB1, ZEB2, TWIST1). (E) Representative fluorescence microscopy images revealing E-cadherin and Vimentin expression patterns in TAMR and ADR cells treated with ITGA11 or EZH2. (F, G) KD of ITGA11, SUZ12, or EZH2 inhibits migratory ability of TAMR and ADR cells, revealed by wound healing assay (F) and transwell migration assay (G). The graphs represent the quantification of wound closure measuring the distance between wound edges using Image J software in the wound healing assay, and the number of migrated cells in the transwell migration assay. The scale bar (black) represents 100 μm at an original magnification of 200× for the transwell migration assay. *p < 0.05 compared to siNT-transfected group