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HER2 and EGFR Overexpression Support Metastatic Progression of Prostate Cancer to Bone
Cancer research (Chicago, Ill.), 2017-01, Vol.77 (1), p.74-85
Day, Kathleen C
Lorenzatti Hiles, Guadalupe
Kozminsky, Molly
Dawsey, Scott J
Paul, Alyssa
Broses, Luke J
Shah, Rajal
Kunja, Lakshmi P
Hall, Christopher
Palanisamy, Nallasivam
Daignault-Newton, Stephanie
El-Sawy, Layla
Wilson, Steven James
Chou, Andrew
Ignatoski, Kathleen Woods
Keller, Evan
Thomas, Dafydd
Nagrath, Sunitha
Morgan, Todd
Day, Mark L
2017
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Day, Kathleen C
Lorenzatti Hiles, Guadalupe
Kozminsky, Molly
Dawsey, Scott J
Paul, Alyssa
Broses, Luke J
Shah, Rajal
Kunja, Lakshmi P
Hall, Christopher
Palanisamy, Nallasivam
Daignault-Newton, Stephanie
El-Sawy, Layla
Wilson, Steven James
Chou, Andrew
Ignatoski, Kathleen Woods
Keller, Evan
Thomas, Dafydd
Nagrath, Sunitha
Morgan, Todd
Day, Mark L
Titel
HER2 and EGFR Overexpression Support Metastatic Progression of Prostate Cancer to Bone
Ist Teil von
Cancer research (Chicago, Ill.), 2017-01, Vol.77 (1), p.74-85
Ort / Verlag
United States: American Association for Cancer Research, Inc
Erscheinungsjahr
2017
Quelle
MEDLINE
Beschreibungen/Notizen
Activation of the EGF receptors EGFR (ErbB1) and HER2 (ErbB2) drives the progression of multiple cancer types through complex mechanisms that are still not fully understood. In this study, we report that HER2 expression is elevated in bone metastases of prostate cancer independently of gene amplification. An examination of HER2 and NF-κB receptor (RANK) coexpression revealed increased levels of both proteins in aggressive prostate tumors and metastatic deposits. Inhibiting HER2 expression in bone tumor xenografts reduced proliferation and RANK expression while maintaining EGFR expression. In examining the role of EGFR in tumor-initiating cells (TIC), we found that EGFR expression was required for primary and secondary sphere formation of prostate cancer cells. EGFR expression was also observed in circulating tumor cells (CTC) during prostate cancer metastasis. Dual inhibition of HER2 and EGFR resulted in significant inhibition of tumor xenograft growth, further supporting the significance of these receptors in prostate cancer progression. Overall, our results indicate that EGFR promotes survival of prostate TIC and CTC that metastasize to bone, whereas HER2 supports the growth of prostate cancer cells once they are established at metastatic sites. Cancer Res; 77(1); 74-85. ©2016 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 0008-5472
eISSN: 1538-7445
DOI: 10.1158/0008-5472.can-16-1656
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5214538
Format
–
Schlagworte
Animals
,
Blotting, Western
,
Bone cancer
,
Bone Neoplasms - secondary
,
Bone tumors
,
Cell Line, Tumor
,
Disease Progression
,
Epidermal growth factor receptors
,
ErbB Receptors - biosynthesis
,
ErbB-1 protein
,
ErbB-2 protein
,
Flow Cytometry
,
Gene amplification
,
Heterografts
,
Humans
,
Immunohistochemistry
,
In Situ Hybridization, Fluorescence
,
Inhibition
,
Male
,
Metastases
,
Metastasis
,
Mice
,
Mice, Inbred NOD
,
Mice, SCID
,
Neoplasm Invasiveness - pathology
,
Neoplastic Cells, Circulating - pathology
,
Neoplastic Stem Cells - pathology
,
NF-κB protein
,
Prostate cancer
,
Prostatic Neoplasms - pathology
,
Proteins
,
Receptor, ErbB-2 - biosynthesis
,
Tissue Array Analysis
,
Tumor cells
,
Tumors
,
Up-Regulation
,
Xenografts
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