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α3 Chains of type V collagen regulate breast tumour growth via glypican-1

Author

Listed:
  • Guorui Huang

    (University of Wisconsin School of Medicine and Public Health)

  • Gaoxiang Ge

    (University of Wisconsin School of Medicine and Public Health
    Present address: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China)

  • Valerio Izzi

    (Centre of Excellence in Cell-Extracellular Matrix Research and Biocenter Oulu, Faculty of Biochemistry and Molecular Medicine, University of Oulu)

  • Daniel S. Greenspan

    (University of Wisconsin School of Medicine and Public Health)

Abstract

Pericellular 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.

Suggested Citation

  • Guorui Huang & Gaoxiang Ge & Valerio Izzi & Daniel S. Greenspan, 2017. "α3 Chains of type V collagen regulate breast tumour growth via glypican-1," Nature Communications, Nature, vol. 8(1), pages 1-17, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14351
    DOI: 10.1038/ncomms14351
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