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Hepatocyte Growth Factor Induces Invasion and Migration of Ovarian Cancer Cells by Decreasing the Expression of E‐cadherin, β‐catenin, and Caveolin‐1
Author(s) -
Hu Jun,
Shao Shujuan,
Song Yang,
Zhao Jinyao,
Dong Yan,
Gong Linlin,
Yang Peiman
Publication year - 2010
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.21147
Subject(s) - hepatocyte growth factor , ovarian cancer , cadherin , metastasis , caveolin 1 , catenin , cancer research , biology , cell migration , cell , cell growth , downregulation and upregulation , chemistry , cancer , wnt signaling pathway , microbiology and biotechnology , medicine , signal transduction , gene , receptor , genetics , biochemistry
Distant metastases are unusual occurrences at presentation and during the progression of epithelial ovarian cancer. There are no good clinical predictors of this phenomenon. In this study, we examined the role of hepatocyte growth factor (HGF) in cell metastasis in ovarian cancer HO8910 cells. We found that HGF has functions in biological processes essential to metastasis, including morphological remodeling, invasion and migration ( P = 0.000, P = 0.001). Western blotting showed that in HGF treated group, the expression of E‐cadherin, β‐catenin, and caveolin‐1 was decreased as compared with the control group ( P = 0.000, P = 0.002, P = 0.000). Immunofluorescence staining demonstrated that the population of E‐cadherin, β‐catenin, and caveolin‐1 at the cell membrane was downregulated. Reverse transcriptase polymerase chain reaction analysis revealed the decreased expression of E‐cadherin, β‐catenin, and caveolin‐1 at the mRNA level. Our data indicated that HGF leads to downregulation of E‐cadherin, β‐catenin, and caveolin‐1, disassembly of cell–cell contacts, and invasion and migration enhancement in human ovarian cancer cells. Anat Rec 293:1125–1133, 2010. © 2010 Wiley‐Liss, Inc.