Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11803
Title: P21-activated kinase 1 promotes colorectal cancer survival by up-regulation of hypoxia-inducible factor-1α.
Authors: Liu, Kevin H;Huynh, Nhi;Patel, Oneel;Shulkes, Arthur;Baldwin, Graham S;He, Hong
Affiliation: Department of Surgery, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australia.
Issue Date: 26-Jun-2013
Citation: Cancer Letters 2013; 340(1): 22-9
Abstract: P21 activated kinase 1 (PAK1) enhances colorectal cancer (CRC) progression by stimulating Wnt/β-catenin and Ras oncogene, which promote CRC survival via stimulation of hypoxia-inducible factor 1α (HIF-1α). The aim of this study was to assess the mechanism involved in the stimulation by PAK1 of CRC survival. PAK1 promoted CRC cell survival by up-regulation of HIF-1α. PAK1 was over-expressed and hyper-activated in tumors of ApcΔ(14/+) mice, which was correlated with over-expression of HIF-1α and β-catenin. Inhibition of PAK1 decreased tumor growth and the expression of HIF-1α and β-catenin in tumors of ApcΔ(14/+) mice, and suppressed xenograft tumor survival in SCID mice. These findings indicate that PAK1 stimulates CRC survival by up-regulation of HIF-1α.
Internal ID Number: 23811286
URI: http://ahro.austin.org.au/austinjspui/handle/1/11803
DOI: 10.1016/j.canlet.2013.06.024
URL: http://www.ncbi.nlm.nih.gov/pubmed/23811286
Type: Journal Article
Subjects: CRC
HIF-1α
PAK1
β-Catenin
Animals
Cell Hypoxia
Cell Survival
Colorectal Neoplasms.enzymology.pathology.therapy
Enzyme Activation
Female
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
HCT116 Cells
HT29 Cells
Humans
Hypoxia-Inducible Factor 1, alpha Subunit.genetics.metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, SCID
RNA, Small Interfering.genetics
Tumor Burden
Up-Regulation
Vascular Endothelial Growth Factor A.secretion
beta Catenin.metabolism
p21-Activated Kinases.antagonists & inhibitors.physiology
Appears in Collections:Journal articles

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