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δ‐catenin overexpression promotes angiogenic potential of CWR22Rv‐1 prostate cancer cells via HIF‐1α and VEGF
Author(s) -
He Yongfeng,
Kim Hangun,
Ryu Taeyong,
Kang Youra,
Kim Jeong-Ae,
Kim Bo-Hyun,
Lee Jae-Hyuk,
Kang Keonwook,
Lu Qun,
Kim Kwonseop
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.11.024
Subject(s) - catenin , prostate cancer , gene knockdown , vascular endothelial growth factor , cancer research , beta catenin , hypoxia inducible factors , hypoxia (environmental) , chemistry , vegf receptors , angiogenesis , prostate , biology , cancer , wnt signaling pathway , medicine , microbiology and biotechnology , signal transduction , apoptosis , gene , biochemistry , organic chemistry , oxygen
This study revealed that CWR22Rv‐1 cells overexpressing δ‐catenin display bigger tumor formation and higher angiogenic potentials than their matched control cells in the CAM assay. In addition, δ‐catenin overexpression in CWR22Rv‐1 cells results in increased hypoxia‐inducible factor 1‐alpha (HIF‐1α and vascular endothelial growth factor (VEGF) expression. Furthermore, δ‐catenin overexpression was found to enhance nuclear distribution of both β‐catenin and HIF‐1α in hypoxic condition, which is diminished by knockdown of δ‐catenin. Our current study adds novel evidence regarding contribution of δ‐catenin to the progression of prostate cancer.