The Cell Surface Glycoprotein CUB Domain-containing Protein 1 (CDCP1) Contributes to Epidermal Growth Factor Receptor-mediated Cell Migration

Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-ind...

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Published inThe Journal of biological chemistry Vol. 287; no. 13; pp. 9792 - 9803
Main Authors Dong, Ying, He, Yaowu, de Boer, Leonore, Stack, M. Sharon, Lumley, John W., Clements, Judith A., Hooper, John D.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 23.03.2012
American Society for Biochemistry and Molecular Biology
Subjects
Antigens, CD - biosynthesis
Antigens, CD - genetics
Antigens, Neoplasm
Antineoplastic Agents - pharmacology
CDCP1
Cell Adhesion Molecules - biosynthesis
Cell Adhesion Molecules - genetics
Cell Biology
Cell Line, Tumor
Cell Migration
Cell Movement
Drug Resistance, Neoplasm - drug effects
Drug Resistance, Neoplasm - genetics
Epidermal Growth Factor - genetics
Epidermal Growth Factor - metabolism
Epidermal Growth Factor Receptor (egfr)
ErbB Receptors - genetics
ErbB Receptors - metabolism
Female
Gene Expression Regulation, Neoplastic
Humans
Intercellular Junctions - genetics
Intercellular Junctions - metabolism
Intercellular Junctions - pathology
MAP Kinase Signaling System - drug effects
MAP Kinase Signaling System - genetics
Mutation
Neoplasm Proteins - biosynthesis
Neoplasm Proteins - genetics
Ovarian Cancer
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Protein Structure
Pseudopodia - genetics
Pseudopodia - metabolism
Pseudopodia - pathology
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
RNA, Neoplasm - biosynthesis
RNA, Neoplasm - genetics
Up-Regulation
Cell Migration
Ovarian Cancer
CDCP1
Protein Structure
Epidermal Growth Factor Receptor (egfr)
Cell Biology
Online AccessGet full text

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Abstract Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-induced cell migration. We show that signaling via EGF/EGFR induces migration of ovarian cancer Caov3 and OVCA420 cells with concomitant up-regulation of CDCP1 mRNA and protein. Consistent with a role in cell migration CDCP1 relocates from cell-cell junctions to punctate structures on filopodia after activation of EGFR. Significantly, disruption of CDCP1 either by silencing or the use of a function blocking antibody efficiently reduces EGF/EGFR-induced cell migration of Caov3 and OVCA420 cells. We also show that up-regulation of CDCP1 is inhibited by pharmacological agents blocking ERK but not Src signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce increased expression of CDCP1. Our immunohistochemical analysis of benign, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed during progression of this cancer. These data highlight a novel role for CDCP1 in EGF/EGFR-induced cell migration and indicate that targeting of CDCP1 may be a rational approach to inhibit progression of cancers driven by EGFR signaling including those resistant to anti-EGFR drugs because of activating mutations in the RAS/RAF/MEK/ERK pathway. Epidermal growth factor (EGF) activates EGF receptor (EGFR) to promote cell migration and cancer. EGF/EGFR up-regulates the cell surface glycoprotein CDCP1, and blockade of CDCP1 reduces EGF/EGFR-induced migration of ovarian cancer cells lines. CDCP1 is expressed by ovarian tumors. CDCP1 contributes to EGF/EGFR-induced cell migration. Targeting of CDCP1 may be a rational approach to inhibit cancers mediated by EGFR.
AbstractList Background: Epidermal growth factor (EGF) activates EGF receptor (EGFR) to promote cell migration and cancer. Results: EGF/EGFR up-regulates the cell surface glycoprotein CDCP1, and blockade of CDCP1 reduces EGF/EGFR-induced migration of ovarian cancer cells lines. CDCP1 is expressed by ovarian tumors. Conclusion: CDCP1 contributes to EGF/EGFR-induced cell migration. Significance: Targeting of CDCP1 may be a rational approach to inhibit cancers mediated by EGFR. Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-induced cell migration. We show that signaling via EGF/EGFR induces migration of ovarian cancer Caov3 and OVCA420 cells with concomitant up-regulation of CDCP1 mRNA and protein. Consistent with a role in cell migration CDCP1 relocates from cell-cell junctions to punctate structures on filopodia after activation of EGFR. Significantly, disruption of CDCP1 either by silencing or the use of a function blocking antibody efficiently reduces EGF/EGFR-induced cell migration of Caov3 and OVCA420 cells. We also show that up-regulation of CDCP1 is inhibited by pharmacological agents blocking ERK but not Src signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce increased expression of CDCP1. Our immunohistochemical analysis of benign, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed during progression of this cancer. These data highlight a novel role for CDCP1 in EGF/EGFR-induced cell migration and indicate that targeting of CDCP1 may be a rational approach to inhibit progression of cancers driven by EGFR signaling including those resistant to anti-EGFR drugs because of activating mutations in the RAS/RAF/MEK/ERK pathway.
Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-induced cell migration. We show that signaling via EGF/EGFR induces migration of ovarian cancer Caov3 and OVCA420 cells with concomitant up-regulation of CDCP1 mRNA and protein. Consistent with a role in cell migration CDCP1 relocates from cell-cell junctions to punctate structures on filopodia after activation of EGFR. Significantly, disruption of CDCP1 either by silencing or the use of a function blocking antibody efficiently reduces EGF/EGFR-induced cell migration of Caov3 and OVCA420 cells. We also show that up-regulation of CDCP1 is inhibited by pharmacological agents blocking ERK but not Src signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce increased expression of CDCP1. Our immunohistochemical analysis of benign, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed during progression of this cancer. These data highlight a novel role for CDCP1 in EGF/EGFR-induced cell migration and indicate that targeting of CDCP1 may be a rational approach to inhibit progression of cancers driven by EGFR signaling including those resistant to anti-EGFR drugs because of activating mutations in the RAS/RAF/MEK/ERK pathway.
Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes a number of malignancies including ovarian cancer. We have identified the cell surface glycoprotein CDCP1 as a key regulator of EGF/EGFR-induced cell migration. We show that signaling via EGF/EGFR induces migration of ovarian cancer Caov3 and OVCA420 cells with concomitant up-regulation of CDCP1 mRNA and protein. Consistent with a role in cell migration CDCP1 relocates from cell-cell junctions to punctate structures on filopodia after activation of EGFR. Significantly, disruption of CDCP1 either by silencing or the use of a function blocking antibody efficiently reduces EGF/EGFR-induced cell migration of Caov3 and OVCA420 cells. We also show that up-regulation of CDCP1 is inhibited by pharmacological agents blocking ERK but not Src signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce increased expression of CDCP1. Our immunohistochemical analysis of benign, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed during progression of this cancer. These data highlight a novel role for CDCP1 in EGF/EGFR-induced cell migration and indicate that targeting of CDCP1 may be a rational approach to inhibit progression of cancers driven by EGFR signaling including those resistant to anti-EGFR drugs because of activating mutations in the RAS/RAF/MEK/ERK pathway. Epidermal growth factor (EGF) activates EGF receptor (EGFR) to promote cell migration and cancer. EGF/EGFR up-regulates the cell surface glycoprotein CDCP1, and blockade of CDCP1 reduces EGF/EGFR-induced migration of ovarian cancer cells lines. CDCP1 is expressed by ovarian tumors. CDCP1 contributes to EGF/EGFR-induced cell migration. Targeting of CDCP1 may be a rational approach to inhibit cancers mediated by EGFR.
Author de Boer, Leonore
Dong, Ying
He, Yaowu
Lumley, John W.
Clements, Judith A.
Hooper, John D.
Stack, M. Sharon
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  givenname: M. Sharon
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  givenname: John W.
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  surname: Hooper
  fullname: Hooper, John D.
  email: jhooper@mmri.mater.org.au
  organization: Mater Medical Research Institute, South Brisbane, Queensland 4101, Australia
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22315226$$D View this record in MEDLINE/PubMed
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Issue 13
Keywords Cell Migration
Ovarian Cancer
CDCP1
Protein Structure
Epidermal Growth Factor Receptor (egfr)
Cell Biology
Language English
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Present address: Dept. of Chemistry and Biochemistry, Harper Cancer Research Institute, University of Notre Dame, Notre Dame, IN 46556.
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SSID ssj0000491
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Snippet Epidermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell migration, and aberrant signaling via this system promotes...
Background: Epidermal growth factor (EGF) activates EGF receptor (EGFR) to promote cell migration and cancer. Results: EGF/EGFR up-regulates the cell surface...
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crossref
pubmed
elsevier
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StartPage 9792
SubjectTerms Antigens, CD - biosynthesis
Antigens, CD - genetics
Antigens, Neoplasm
Antineoplastic Agents - pharmacology
CDCP1
Cell Adhesion Molecules - biosynthesis
Cell Adhesion Molecules - genetics
Cell Biology
Cell Line, Tumor
Cell Migration
Cell Movement
Drug Resistance, Neoplasm - drug effects
Drug Resistance, Neoplasm - genetics
Epidermal Growth Factor - genetics
Epidermal Growth Factor - metabolism
Epidermal Growth Factor Receptor (egfr)
ErbB Receptors - genetics
ErbB Receptors - metabolism
Female
Gene Expression Regulation, Neoplastic
Humans
Intercellular Junctions - genetics
Intercellular Junctions - metabolism
Intercellular Junctions - pathology
MAP Kinase Signaling System - drug effects
MAP Kinase Signaling System - genetics
Mutation
Neoplasm Proteins - biosynthesis
Neoplasm Proteins - genetics
Ovarian Cancer
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Protein Structure
Pseudopodia - genetics
Pseudopodia - metabolism
Pseudopodia - pathology
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
RNA, Neoplasm - biosynthesis
RNA, Neoplasm - genetics
Up-Regulation
Title The Cell Surface Glycoprotein CUB Domain-containing Protein 1 (CDCP1) Contributes to Epidermal Growth Factor Receptor-mediated Cell Migration
URI https://dx.doi.org/10.1074/jbc.M111.335448
https://www.ncbi.nlm.nih.gov/pubmed/22315226
https://search.proquest.com/docview/948911871
https://pubmed.ncbi.nlm.nih.gov/PMC3322992
Volume 287
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