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Cited by 183Cell Adhesion Molecules ResearchProtease and Inhibitor MechanismsBone and Dental Protein Studies

CD151 Accelerates Breast Cancer by Regulating α6 Integrin Function, Signaling, and Molecular Organization

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Yang, Xiuwei H., Richardson, Andrea L., Torres-Arzayus, Maria I., Zhou, Pengcheng, Sharma, Chandan, Kazarov, Alexander R., Andzelm, Milena M., Strominger, Jack L. +2 more·2008·Cancer Research
DOI 10.1158/0008-5472.can-07-2949PMC PMC4764302

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Abstract

CD151, a master regulator of laminin-binding integrins (alpha(6)beta(4), alpha(6)beta(1), and alpha(3)beta(1)), assembles these integrins into complexes called tetraspanin-enriched microdomains. CD151 protein expression is elevated in 31% of human breast cancers and is even more elevated in high-grade (40%) and estrogen receptor-negative (45%) subtypes. The latter includes triple-negative (estrogen receptor, progesterone receptor, and HER2 negative) basal-like tumors. CD151 ablation markedly reduced basal-like mammary cell migration, invasion, spreading, and signaling (through FAK, Rac1, and lck) while disrupting epidermal growth factor receptor (EGFR)-alpha(6) integrin collaboration. Underlying these defects, CD151 ablation redistributed alpha(6)beta(4) integrins subcellularly and severed molecular links between integrins and tetraspanin-enriched microdomains. In a prototypical basal-like mammary tumor line, CD151 ablation notably delayed tumor progression in ectopic and orthotopic xenograft models. These results (a) establish that CD151-alpha(6) integrin complexes play a functional role in basal-like mammary tumor progression; (b) emphasize that alpha(6) integrins function via CD151 linkage in the context of tetraspanin-enriched microdomains; and (c) point to potential relevance of CD151 as a high-priority therapeutic target, with relative selectivity (compared with laminin-binding integrins) for pathologic rather than normal physiology.

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  • ITGB1 and CD151 are pro-tumorigenic by enhancing cell migration and stromal invasion.

    “ITGB1 and CD151 are known to be pro-tumorigenic by enhancing cell migration and stromal invasion (Reuter et al., 2009, White et al., 2004, Yang et al., 2008, Zijlstra et al., 2008).”

    From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Yang et al., 2008

    The Results report that CD151 silencing reduced mammary-cell migration and Matrigel invasion, and the conclusion links CD151 to tumor progression. The paper associates CD151 with β1-containing integrins, but its functional findings focus on α6 integrin and do not establish that ITGB1 itself enhances migration or stromal invasion. The invasion assay used Matrigel, not stroma. (LLM, conf=0.87)

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1 of the 53 references couldn’t be matched to a known paper.

Research works printed but not linked: 3

  1. Lammerding J, Kazarov AR, Huang H, Lee RT, Hemler ME. Tetraspanin CD151 regulates a 6 h 1 integrin adhe- sion strengthening. Proc Natl Acad Sci U S A 2003;100: 7616-21.
  2. Belkin AM, Stepp MA. Integrins as receptors for laminins. Microsc Res Tech 2000;51:280-301.
  3. Lau LM, Wee JL, Wright MD, et al. The tetraspanin superfamily member, CD151 regulates outside-in integ- rin a IIb h 3 signalling and platelet function. Blood 2004;104: 104:2368-75.

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Authors
Yang, X. H., Richardson, A. L., Torres-Arzayus, M. I., Zhou, P., Sharma, C., Kazarov, A. R., Andzelm, M. M., Strominger, J. L., Brown, M., & Hemler, M. E.
Affiliations
  • Harvard University (US)
  • Brigham and Women's Hospital (US)
  • 2Medical Oncology, and
ORCID
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2008-05-01
Volume
68
Issue
9
Pages
3204-3213
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
DOI
10.1158/0008-5472.can-07-2949
PMC
PMC4764302
OpenAlex
W2102040455
Cited by
183
References
53
Citations by year
2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 13 · 2020: 8 · 2019: 7 · 2018: 7 · 2017: 9 · 2016: 8 · 2015: 14 · 2014: 7 · 2013: 21 · 2012: 22
FWCI
11.91
Type
journal article
Language
en
Open access
Locations
  • Cancer Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Breast Cancer Research Foundation
  • National Institutes of Health
  • National Cancer Institute (CA-42368, R01CA042368)
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
Keywords
CD151, CD49f, breast cancer, basal-like breast cancer, triple-negative breast cancer, tetraspanin-enriched microdomains, laminin-binding integrins, integrin signaling, tumor progression, EGFR, focal adhesion kinase, Rac1, Lck, tumor cell migration and invasion, therapeutic target
MeSH terms
Animals, Breast Neoplasms, Cell Adhesion, Cell Movement, Epidermal Growth Factor, Humans, Mice, Nude, Neoplasm Invasiveness, Protein Binding, Tissue Distribution, Transplantation, Heterologous, Tumor Cells, Cultured, Signal Transduction, Antigens, CD, Gene Expression Regulation, Neoplastic, Disease Progression, Integrin alpha6, Mammary Glands, Human, Mice, Tetraspanin 24

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