Fig. 2
E2F7, NFIA, DEK, SMAD2, SMARCA1, ASCL1 and TRPS1 - roles in endocrine resistance. a Cellular viability is significantly reduced after siRNA knockdown of E2F7, NFIA, DEK, SMAD2, ASCL1 and TRPS1 in endocrine resistant LY2 cells with no significant changes observed with siSMARCA1. b Anchorage independent growth of LY2 cells was reduced following siRNA transfection with NFIA, SMAD2, SMARCA1, ASCL1 and TRPS1. Growth was increased with siDEK transfection and no significant changes were observed with siE2F7. Representative images of cells’ anchorage independent growth. c Mammosphere forming efficiency in first and second generation of mammospheres was significantly reduced following knockdown of E2F7, NFIA, DEK, SMAD2, SMARCA1, ASCL1 and TRPS1. d Representative images of acini formation from LY2 cells following siRNA transfection with E2F7, NFIA, DEK, SMAD2, SMARCA1, ASCL1 and TRPS1 showed more organised acini with superior apico-basolateral structure compared to siScramble cells. e Flow cytometry analysis of CD44 and CD24 expression in LY2 cells transfected with siRNA against E2F7, NFIA, DEK, SMAD2, SMARCA1, ASCL1 and TRPS1. The results showed a significant reduction in CD24−CD44+ (stem cell-like). f Migratory ability of the LY2 cells was significantly reduced following siRNA transfection with E2F7, NFIA, DEK, SMAD2, SMARCA1 ASCL1 and TRPS1. Representative images of cellular migration shown. All results are expressed as mean ± SEM, n = 3, p < 0.05, normalised to siScramble
