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Distinct regulatory effect of the p34(SEI-1) oncoprotein on cancer metastasis in HER2/neu-positive and -negative cells

Authors
Jung, SamilOhk, JiyeonJeong, DongjunLi, ChengpingLee, SoonduckDuan, JingjingKim, ChangjinLim, Jong-SeokYang, YoungKim, Keun-IlLee, Myeong-Sok
Issue Date
Jul-2014
Publisher
SPANDIDOS PUBL LTD
Keywords
metastasis; 34-kD protein encoding SEI-1 gene; human epidermal growth factor receptor 2; phosphoinositide-3 kinase/serine/threonine-specific protein kinase; integrin-linked kinase
Citation
INTERNATIONAL JOURNAL OF ONCOLOGY, v.45, no.1, pp 189 - 196
Pages
8
Journal Title
INTERNATIONAL JOURNAL OF ONCOLOGY
Volume
45
Number
1
Start Page
189
End Page
196
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10861
DOI
10.3892/ijo.2014.2403
ISSN
1019-6439
1791-2423
Abstract
The p34(SEI-1) oncoprotein is involved in a transcriptional regulation, cell cycle regulation, apoptosis, development and many other important cellular functions. Our present study suggests that p34(SEI-1) can promote metastasis by enhancing migration and invasion of cancer cells. Consistently, p34(SEI-1) expression was found to be increased as the tumor invasiveness progressed in human breast tissues. p34(SEI-1) may promote cancer metastasis by activating the PI3K/AKT signaling pathway. In this process, p34(SEI-1) activates two different serine/threonine kinases, AKT or ILK, depending on the expression status of HER2/neu oncogene. In HER2/neu suppressed cancer cells, p34(SEI-1) promoted metastasis mainly by activating AKT via phosphorylation of the 473 serine residue. In HER2/neu expressing cancer cells, p34(SEI-1) overexpression downregulates HER2/neu expression, leading to the activation of another crucial serine/threonine kinase ILK due to phosphorylation of the 178 threonine residue instead of AKT. These results suggest that p34(SEI-1) affects cancer metastasis by regulating two different signaling pathways depending on the HER2/neu expression level, in which AKT and ILK modulation can be stimulated by p34(SEI-1) overexpression.
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