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Compared to other cancers affecting women, breast cancer is significantlyassociated with alcohol consumption. However, the principles underlying the carcinogenesisof alcohol-induced breast cancer and the related metastatic mechanisms have yetto be established. To observe the effect of alcohol on the growth regulation inbreast cancer cells, we identified differentially expressed proteins in alcohol-exposedhuman breast cancer T47D cells using gel-based proteomics analysis. The expressionof c-ros receptor tyrosine kinase (ROS1) was increased and activated by autophosphorylation,thereby activating mitogen- and stress-activated protein kinase 1 (MSK1) throughthe mitogen‑activated protein kinase (MAPK) pathway; activated MSK1, in turn,phosphorylated histone 3 serine 10 (H3S10p) residues in the nucleus. The increasein H3S10 phosphorylation consequently increased the level of expression of immediate-earlygene such as c-fos. This study demonstrated that when breast cancer cells areexposed to alcohol, phosphorylated ROS1 activates MSK1 via Erk1/2 in the MAPKpathway, which then induces modifications to histone residues that regulate geneexpression by 14-3-3 protein recruitment, leading to a lack of control of breastcancer cell proliferation.

oncology reports

Effects of the activated mitogen-activated protein kinase pathway via the c-ros receptor tyrosine kinase on the T47D breast cancer cell line following alcohol exposure