EGFR and breast carcinoma: Strikingly, the decreased invasiveness was re-increased by the transient transfection of the shRNA-resistant HDAC3wt plasmid, but not by rshHDAC3Y321/331, strongly confirming that EGFR–c-Src mediated HDAC3 phosphorylation at Y321 and 331 was crucial for the invasion of breast cancer cells.