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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

Title
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
Author
채영규
Keywords
breast cancer; alcohol; receptor tyrosine kinase; mitogen-activated protein kinase pathway; histone phosphorylation; TRANSFORMED MOUSE FIBROBLASTS; HISTONE H3 PHOSPHORYLATION; B-INDUCED PHOSPHORYLATION; GENE-EXPRESSION; SER-10 PHOSPHORYLATION; ACUTE ETHANOL; MAP KINASE; P38 MAPK; MECHANISMS; STRESS
Issue Date
2013-03
Publisher
SPANDIDOS PUBL LTD, POB 18179, ATHENS, 116 10, GREECE
Citation
ONCOLOGY REPORTS, 2013, 29(3), p.868-874
Abstract
Compared to other cancers affecting women, breast cancer is significantly associated with alcohol consumption. However, the principles underlying the carcinogenesis of alcohol-induced breast cancer and the related metastatic mechanisms have yet to be established. To observe the effect of alcohol on the growth regulation in breast cancer cells, we identified differentially expressed proteins in alcohol-exposed human breast cancer T47D cells using gel-based proteomics analysis. The expression of c-ros receptor tyrosine kinase (ROS1) was increased and activated by autophosphorylation, thereby activating mitogen- and stress-activated protein kinase 1 (MSK1) through the mitogen-activated protein kinase (MAPK) pathway; activated MSK1, in turn, phosphorylated histone 3 serine 10 (H3S10p) residues in the nucleus. The increase in H3S10 phosphorylation consequently increased the level of expression of immediate-early gene such as c-fos. This study demonstrated that when breast cancer cells are exposed to alcohol, phosphorylated ROS1 activates MSK1 via ERK1/2 in the MAPK pathway, which then induces modifications to histone residues that regulate gene expression by 14-3-3 protein recruitment, leading to a lack of control of breast cancer cell proliferation.
URI
https://www.spandidos-publications.com/10.3892/or.2012.2209http://hdl.handle.net/20.500.11754/49209
ISSN
1021-335X
DOI
10.3892/or.2012.2209
Appears in Collections:
GRADUATE SCHOOL[S](대학원) > BIONANOTECHNOLOGY(바이오나노학과) > Articles
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