|
|
α3 chains of type V collagen regulate breast tumour growth via glypican-1 |
|---|---|
| Author: | Huang, Guorui1; Ge, Gaoxiang1,2; Izzi, Valerio3; |
| Organizations: |
1Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53705, USA 2Present address: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China 3Centre of Excellence in Cell-Extracellular Matrix Research and Biocenter Oulu, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Aapistie 5, Oulu 92100, Finland |
| Format: | article |
| Version: | published version |
| Access: | open |
| Online Access: | PDF Full Text (PDF, 3.8 MB) |
| Persistent link: | http://urn.fi/urn:nbn:fi-fe201703315928 |
| Language: | English |
| Published: |
Springer Nature,
2017
|
| Publish Date: | 2017-03-31 |
| Description: |
AbstractPericellular α3(V) collagen can affect the functioning of cells, such as adipocytes and pancreatic β cells. Here we show that α3(V) chains are an abundant product of normal mammary gland basal cells, and that α3(V) ablation in a mouse mammary tumour model inhibits mammary tumour progression by reducing the proliferative potential of tumour cells. These effects are shown to be primarily cell autonomous, from loss of α3(V) chains normally produced by tumour cells, in which they affect growth by enhancing the ability of cell surface proteoglycan glypican-1 to act as a co-receptor for FGF2. Thus, a mechanism is presented for microenvironmental influence on tumour growth. α3(V) chains are produced in both basal-like and luminal human breast tumours, and its expression levels are tightly coupled with those of glypican-1 across breast cancer types. Evidence indicates α3(V) chains as potential targets for inhibiting tumour growth and as markers of oncogenic transformation. see all
|
| Series: |
Nature communications |
| ISSN: | 2041-1723 |
| ISSN-E: | 2041-1723 |
| ISSN-L: | 2041-1723 |
| Volume: | 8 |
| Article number: | 14351 |
| DOI: | 10.1038/ncomms14351 |
| OADOI: | https://oadoi.org/10.1038/ncomms14351 |
| Type of Publication: |
A1 Journal article – refereed |
| Field of Science: |
1182 Biochemistry, cell and molecular biology 3111 Biomedicine 3122 Cancers |
| Subjects: | |
| Funding: |
We also thank the
University of Wisconsin Carbone Cancer Center (UWCCC) for subsidized (NIH/NCI
P30CA014520—UWCCC support grant) use of Shared Resources. This work was
supported by a Centre of Excellence Grant 284606 from the Academy of Finland (V.I.)
and by NIH grants R01-AR47746 and PO1AI084853 (D.S.G.) |
| Academy of Finland Grant Number: |
284606 |
| Detailed Information: |
284606 (Academy of Finland Funding decision) |
| Copyright information: |
© The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0
International License. The images or other third party material in this
article are included in the article’s Creative Commons license, unless indicated otherwise
in the credit line; if the material is not included under the Creative Commons license,
users will need to obtain permission from the license holder to reproduce the material.
To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
|
https://creativecommons.org/licenses/by/4.0/ |