N-α-acetyltransferase 10 protein suppresses cancer cell metastasis by binding PIX proteins and inhibiting Cdc42/Rac1 activity

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Sökning: WFRF:(Cheng Sheng Yao) > (2010-2014) > N-α-acetyltransfera...

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Fältnamn	Indikatorer	Metadata
000		03199naa a2200589 4500
001		oai:DiVA.org:umu-106964
003		SwePub
008		150813s2011 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1069642 URI
024	7	a https://doi.org/10.1016/j.ccr.2010.11.0102 DOI
040		a (SwePub)umu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Hua, Kuo-Tai4 aut
245	1 0	a N-α-acetyltransferase 10 protein suppresses cancer cell metastasis by binding PIX proteins and inhibiting Cdc42/Rac1 activity
264	1	b Cell Press,c 2011
338		a print2 rdacarrier
520		a N-α-acetyltransferase 10 protein, Naa10p, is an N-acetyltransferase known to be involved in cell cycle control. We found that Naa10p was expressed lower in varieties of malignancies with lymph node metastasis compared with non-lymph node metastasis. Higher Naa10p expression correlates the survival of lung cancer patients. Naa10p significantly suppressed migration, tumor growth, and metastasis independent of its enzymatic activity. Instead, Naa10p binds to the GIT-binding domain of PIX, thereby preventing the formation of the GIT-PIX-Paxillin complex, resulting in reduced intrinsic Cdc42/Rac1 activity and decreased cell migration. Forced expression of PIX in Naa10-transfected tumor cells restored the migration and metastasis ability. We suggest that Naa10p functions as a tumor metastasis suppressor by disrupting the migratory complex, PIX-GIT- Paxillin, in cancer cells.
650	7	a NATURVETENSKAPx Biologix Cellbiologi0 (SwePub)106042 hsv//swe
650	7	a NATURAL SCIENCESx Biological Sciencesx Cell Biology0 (SwePub)106042 hsv//eng
700	1	a Tan, Ching-Ting4 aut
700	1	a Johansson, Gunnaru Graduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei 100, Taiwan4 aut0 (Swepub:umu)gurjon98
700	1	a Lee, Jang-Ming4 aut
700	1	a Yang, Pei-Wen4 aut
700	1	a Lu, Hsin-Yi4 aut
700	1	a Chen, Chi-Kuan4 aut
700	1	a Su, Jen-Liang4 aut
700	1	a Chen, Poshen B4 aut
700	1	a Wu, Yu-Ling4 aut
700	1	a Chi, Chia-Chun4 aut
700	1	a Kao, Hsin-Jung4 aut
700	1	a Shih, Hou-Jung4 aut
700	1	a Chen, Min-Wei4 aut
700	1	a Chien, Ming-Hsien4 aut
700	1	a Chen, Pai-Sheng4 aut
700	1	a Lee, Wei-Jiunn4 aut
700	1	a Cheng, Tsu-Yao4 aut
700	1	a Rosenberger, George4 aut
700	1	a Chai, Chee-Yin4 aut
700	1	a Yang, Chih-Jen4 aut
700	1	a Huang, Ming-Shyan4 aut
700	1	a Lai, Tsung-Ching4 aut
700	1	a Chou, Teh-Ying4 aut
700	1	a Hsiao, Michael4 aut
700	1	a Kuo, Min-Liang4 aut
710	2	a Graduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei 100, Taiwan4 org
773	0	t Cancer Celld : Cell Pressg 19:2, s. 218-231q 19:2<218-231x 1535-6108x 1878-3686
856	4	u http://www.cell.com/article/S1535610810004769/pdf
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-106964
856	4 8	u https://doi.org/10.1016/j.ccr.2010.11.010

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NATURVETENSKAP: NATURVETENSKAP; och Biologi; och Cellbiologi

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Av lärosätet: Umeå universitet

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