HER2 and uPAR cooperativity contribute to metastatic phenotype of HER2-positive breast cancer.
(2015) In Oncoscience 2(3). p.207-224- Abstract
- Human epidermal growth factor receptor type 2 (HER2)-positive breast carcinoma is highly aggressive and mostly metastatic in nature though curable/manageable in part by molecular targeted therapy. Recent evidence suggests a subtype of cells within HER2-positive breast tumors that concomitantly expresses the urokinase plasminogen activator receptor (uPAR) with inherent stem cell/mesenchymal-like properties promoting tumor cell motility and a metastatic phenotype. This HER-positive/uPAR-positive subtype may be partially responsible for the failure of HER2-targeted treatment strategies. Herein we discuss and substantiate the cumulative preclinical and clinical evidence on HER2-uPAR cooperativity in terms of gene co-amplification and/or... (More)
- Human epidermal growth factor receptor type 2 (HER2)-positive breast carcinoma is highly aggressive and mostly metastatic in nature though curable/manageable in part by molecular targeted therapy. Recent evidence suggests a subtype of cells within HER2-positive breast tumors that concomitantly expresses the urokinase plasminogen activator receptor (uPAR) with inherent stem cell/mesenchymal-like properties promoting tumor cell motility and a metastatic phenotype. This HER-positive/uPAR-positive subtype may be partially responsible for the failure of HER2-targeted treatment strategies. Herein we discuss and substantiate the cumulative preclinical and clinical evidence on HER2-uPAR cooperativity in terms of gene co-amplification and/or mRNA/protein co-overexpression. We then propose a regulatory signaling model that we hypothesize to maintain upregulation and cooperativity between HER2 and uPAR in aggressive breast cancer. An improved understanding of the HER2/uPAR interaction in breast cancer will provide critical biomolecular information that may help better predict disease course and response to therapy. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5341095
- author
- Indira Chandran, Vineesh LU ; Eppenberger-Castori, Serenella ; Venkatesh, Thejaswini ; Vine, Kara Lea and Ranson, Marie
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Oncoscience
- volume
- 2
- issue
- 3
- pages
- 207 - 224
- publisher
- Impact Journals
- external identifiers
-
- pmid:25897424
- scopus:84947616846
- ISSN
- 2331-4737
- language
- English
- LU publication?
- yes
- id
- b95c106f-2d5e-48c9-a515-d9465ba66897 (old id 5341095)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25897424?dopt=Abstract
- date added to LUP
- 2016-04-04 09:45:33
- date last changed
- 2022-03-23 07:08:13
@article{b95c106f-2d5e-48c9-a515-d9465ba66897, abstract = {{Human epidermal growth factor receptor type 2 (HER2)-positive breast carcinoma is highly aggressive and mostly metastatic in nature though curable/manageable in part by molecular targeted therapy. Recent evidence suggests a subtype of cells within HER2-positive breast tumors that concomitantly expresses the urokinase plasminogen activator receptor (uPAR) with inherent stem cell/mesenchymal-like properties promoting tumor cell motility and a metastatic phenotype. This HER-positive/uPAR-positive subtype may be partially responsible for the failure of HER2-targeted treatment strategies. Herein we discuss and substantiate the cumulative preclinical and clinical evidence on HER2-uPAR cooperativity in terms of gene co-amplification and/or mRNA/protein co-overexpression. We then propose a regulatory signaling model that we hypothesize to maintain upregulation and cooperativity between HER2 and uPAR in aggressive breast cancer. An improved understanding of the HER2/uPAR interaction in breast cancer will provide critical biomolecular information that may help better predict disease course and response to therapy.}}, author = {{Indira Chandran, Vineesh and Eppenberger-Castori, Serenella and Venkatesh, Thejaswini and Vine, Kara Lea and Ranson, Marie}}, issn = {{2331-4737}}, language = {{eng}}, number = {{3}}, pages = {{207--224}}, publisher = {{Impact Journals}}, series = {{Oncoscience}}, title = {{HER2 and uPAR cooperativity contribute to metastatic phenotype of HER2-positive breast cancer.}}, url = {{http://www.ncbi.nlm.nih.gov/pubmed/25897424?dopt=Abstract}}, volume = {{2}}, year = {{2015}}, }