TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells

doi:10.1371/journal.pone.0023262

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	TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells
	Zhao, Shu-Liang 1; Hong, Jie 1; Xie, Zuo-Quan2 ; Tang, Jie-Ting 1; Su, Wen-Yu 1; Du, Wan 1; Chen, Ying-Xuan 1; Lu, Rong 1; Sun, Dan-Feng 1; Fang, Jing-Yuan 1
刊名	PLOS ONE
	2011-08-03
卷号	6 期号:8
ISSN号	1932-6203
DOI	10.1371/journal.pone.0023262
文献子类	Article
英文摘要	The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells. Overexpression of TRAPPC4 promoted cell viability and caused activated ERK1/2 to increase overall, but especially in the nucleus. TRAPPC4 was expressed more highly in the nucleus of CRC cells than in normal colonic epithelium or adenoma which corresponded with nuclear staining of pERK1/2. We demonstrate here that TRAPPC4 may regulate cell proliferation and apoptosis in CRC by interaction with ERK2 and subsequently phosphorylating ERK1/2 as well as modulating the subcellular location of pERK1/2 to activate the relevant signaling pathway.
资助项目	National Natural Science Foundation of Key Program[30830055] ; National Natural Science Foundation of Youth Program[31000634] ; Shanghai Commission for Science and Technology[10ZR1419000] ; Shanghai Health Bureau for youth[2009032] ; Shanghai Jiao-Tong University School of Medicine Foundation for Science and Technology[09XJ21065]
WOS关键词	SPONDYLOEPIPHYSEAL DYSPLASIA TARDA ; TRAPP COMPLEX ; MAP KINASE ; PROTEIN ; GOLGI ; SYNDECANS ; TRANSPORT ; GENE ; PHOSPHORYLATION ; ARCHITECTURE
WOS研究方向	Science & Technology - Other Topics
语种	英语
出版者	PUBLIC LIBRARY SCIENCE
WOS记录号	WOS:000293558900070
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/278448]
专题	药理学第一研究室中科院受体结构与功能重点实验室新药研究国家重点实验室
通讯作者	Zhao, Shu-Liang
作者单位	1.Shanghai Jiao Tong Univ, Sch Med, Ren Ji Hosp, Shanghai Inst Digest Dis,Dept Gastroenterol, Shanghai 200030, Peoples R China; 2.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Div Antitumor Pharmacol, Shanghai 200031, Peoples R China
推荐引用方式 GB/T 7714	Zhao, Shu-Liang,Hong, Jie,Xie, Zuo-Quan,et al. TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells[J]. PLOS ONE,2011,6(8).
APA	Zhao, Shu-Liang.,Hong, Jie.,Xie, Zuo-Quan.,Tang, Jie-Ting.,Su, Wen-Yu.,...&Fang, Jing-Yuan.(2011).TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells.PLOS ONE,6(8).
MLA	Zhao, Shu-Liang,et al."TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells".PLOS ONE 6.8(2011).