Cited by 212Melanoma and MAPK PathwaysCell Adhesion Molecules ResearchLiver physiology and pathology

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Downregulation of E-cadherin and Desmoglein 1 by autocrine hepatocyte growth factor during melanoma development

Li, Gang, Schaider, Helmut, Satyamoorthy, Kapaettu, Hanakawa, Yasushi, Hashimoto, Koji, Herlyn, Meenhard·2001·Oncogene

DOI 10.1038/sj.onc.1205034

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Abstract

During melanoma development, transformed cells evade keratinocyte-mediated control by downregulating cell adhesion molecules. This study investigated the regulation of cell adhesion by hepatocyte growth factor (HGF) in melanoma. Melanocytes and two melanoma lines, WM164 and WM35, expressed normal level E-cadherin and Desmoglein 1, whereas most melanomas (18 out of 20) expressed no E-cadherin and significantly reduced Desmoglein 1. Overexpression of dominant negative E-cadherin and Desmoglein in melanocytes demonstrated that both molecules contribute to adhesion between melanocytes and keratinocytes. In contrast to melanocytes, most melanomas expressed HGF. All melanocytic cells expressed the HGF receptor c-Met, and autocrine HGF caused constitutive activation of c-Met, MAPK and PI3K. When autocrine activation was induced with HGF-expressing adenovirus, E-cadherin and Desmoglein 1 were decreased in melanocytes, WM164 and WM35. MAPK inhibitor PD98059 and PI3K inhibitor wortmannin partially blocked the downregulation, suggesting that both pathways are involved in this process. c-Met was coimmunoprecipitated with E-cadherin, Desmoglein 1 and Plakoglobin, suggesting that they form a complex (es) that acts to regulate intercellular adhesion. Together, the results indicate that autocrine HGF decouples melanomas from keratinocytes by downregulating E-cadherin and Desmoglein 1, therefore frees melanoma cells from the control by keratinocytes and allows dissemination of the tumor mass.

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Supplementary Figure 2 from Melanoma Proteoglycan Modifies Gene Expression to Stimulate Tumor Cell Motility, Growth, and Epithelial-to-Mesenchymal Transition
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Self-citation
Data from Melanoma Proteoglycan Modifies Gene Expression to Stimulate Tumor Cell Motility, Growth, and Epithelial-to-Mesenchymal Transition
Yang, J., Price, M. A., Li, G. Y., Bar‐Eli, M., Salgia, R., Jagedeeswaran, R., Carlson, J. H., Ferrone, S., Turley, E. A., & McCarthy, J. B. (2023) · doi:10.1158/0008-5472.c.6499020
Self-citation
Supplementary Figure 2 from Melanoma Proteoglycan Modifies Gene Expression to Stimulate Tumor Cell Motility, Growth, and Epithelial-to-Mesenchymal Transition
Yang, J., Price, M. A., Li, G. Y., Bar‐Eli, M., Salgia, R., Jagedeeswaran, R., Carlson, J. H., Ferrone, S., Turley, E. A., & McCarthy, J. B. (2023) · doi:10.1158/0008-5472.22378812
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Self-citation

Authors: Li, G., Schaider, H., Satyamoorthy, K., Hanakawa, Y., Hashimoto, K., & Herlyn, M.
Affiliations: The Wistar Institute (US)
Ehime University (JP)
Corresponding author: Herlyn, Meenhard
ORCID: Schaider, Helmut
Satyamoorthy, Kapaettu
Hashimoto, Koji
Herlyn, Meenhard
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2001-12-06
Volume: 20
Issue: 56
Pages: 8125-8135
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1205034
OpenAlex: W2010980929
Cited by: 212
References: 94
Citations by year: 2025: 2 · 2024: 5 · 2023: 8 · 2022: 2 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 11 · 2016: 8 · 2015: 11 · 2014: 8 · 2013: 9 · 2012: 9
FWCI: 3.15
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: University of Tokyo
National Institutes of Health
National Cancer Institute (R01CA047159, CA 47159, R01CA080999, CA-10815, CA 76674, CA-25874, R01CA076674, CA80999, P01CA025874, P30CA010815)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: melanoma, hepatocyte growth factor, E-cadherin, desmoglein 1, c-Met, autocrine signaling, cell adhesion, plakoglobin, MAPK signaling, PI3K signaling, metastasis, melanocytes
MeSH terms: Cell Adhesion, Cytoskeletal Proteins, Humans, Melanocytes, Melanoma, Precipitin Tests, RNA, Neoplasm, Tumor Cells, Cultured, Signal Transduction, Down-Regulation, Keratinocytes, Cadherins, Hepatocyte Growth Factor, Proto-Oncogene Proteins c-met, Phosphatidylinositol 3-Kinases, Autocrine Communication, Mitogen-Activated Protein Kinases, Desmoplakins, Desmogleins, Desmoglein 1, gamma Catenin

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Downregulation of E-cadherin and Desmoglein 1 by autocrine hepatocyte growth factor during melanoma development

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