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Conference Paper: Modulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment
Title | Modulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment |
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Authors | |
Issue Date | 2015 |
Publisher | American Society of Clinical Oncology. The Journal's web site is located at http://www.jco.org/ |
Citation | The 2015 Breast Cancer Symposium, San Francisco, CA., 25-27 September 2015. In Journal of Clinical Oncology, , v. 33 n. 28 suppl., p. 34 How to Cite? |
Abstract | BACKGROUND: The survival and growth of epithelial carcinoma cells are critically dependent on the interactions with the neighboring stromal cells. Adiponectin, a molecule exclusively produced by adipose tissue, possesses potent anti-inflammatory and anti-tumorigenic activities. Its expression and production are inversely associated with breast cancer risks in pre- and post-menopausal women. Reduced or completely loss of adiponectin expression enhances the development of mammary tumors in MMTV-PyVT mice. Despite these evidences, the mechanisms underlying the anti-breast cancer activity of adiponectin remain poorly understood. METHODS: Adiponectin-deficient MMTV-PyVT mice that show distinct basal epithelial-like features of mammary tumors are used for analyzing the stromal vascular fractions (SVF) of the adipose tissues in tumor microenvironment. RESULTS: Flow cytometric analyses demonstrate that adiponectin deficiency significantly alters the composition of cells in SVF isolated from the mammary adipose tissues. Adiponectin-deficient SVF contribute to the metaplastic features of the basal epithelial-like breast cancers. Co-implantation of SVF derived from adiponectin-deficient mice accelerates mammary tumor development and metastasis in NOD/SCID mice engrafted with MDA-MB-231 human breast cancer cells. Fluorescence Activated Cell Sorting isolates a population of CD44+CD25-CD100+ cells that are enriched in both thymus and SVF of mice lacking the expression of adiponectin. Upregulated CD100 expression interrupts early T-cell development and maturation. In mammary tissues, CD44+CD25-CD100+ cells facilitate the development of metaplastic basal epithelial-like breast cancers. Adiponectin treatment down-regulates CD100 expression, in turn enhancing Notch signaling and T-cell maturation in the thymus, and reduces the accumulation of CD44+CD25-CD100+ cells in the tumor microenvironment. CONCLUSIONS: These results support a pivotal role of adiponectin in mediating the epithelial-stroma crosstalk to prevent mammary carcinogenesis and shed new lights on the development of immuno-therapeutics for breast cancer diseases. |
Description | Poster Session A: Risk Assessment, Prevention, Early Detection, Screening, and Local/Regional Therapy |
Persistent Identifier | http://hdl.handle.net/10722/232561 |
ISSN | 2023 Impact Factor: 42.1 2023 SCImago Journal Rankings: 10.639 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wang, Y | - |
dc.date.accessioned | 2016-09-20T05:30:53Z | - |
dc.date.available | 2016-09-20T05:30:53Z | - |
dc.date.issued | 2015 | - |
dc.identifier.citation | The 2015 Breast Cancer Symposium, San Francisco, CA., 25-27 September 2015. In Journal of Clinical Oncology, , v. 33 n. 28 suppl., p. 34 | - |
dc.identifier.issn | 0732-183X | - |
dc.identifier.uri | http://hdl.handle.net/10722/232561 | - |
dc.description | Poster Session A: Risk Assessment, Prevention, Early Detection, Screening, and Local/Regional Therapy | - |
dc.description.abstract | BACKGROUND: The survival and growth of epithelial carcinoma cells are critically dependent on the interactions with the neighboring stromal cells. Adiponectin, a molecule exclusively produced by adipose tissue, possesses potent anti-inflammatory and anti-tumorigenic activities. Its expression and production are inversely associated with breast cancer risks in pre- and post-menopausal women. Reduced or completely loss of adiponectin expression enhances the development of mammary tumors in MMTV-PyVT mice. Despite these evidences, the mechanisms underlying the anti-breast cancer activity of adiponectin remain poorly understood. METHODS: Adiponectin-deficient MMTV-PyVT mice that show distinct basal epithelial-like features of mammary tumors are used for analyzing the stromal vascular fractions (SVF) of the adipose tissues in tumor microenvironment. RESULTS: Flow cytometric analyses demonstrate that adiponectin deficiency significantly alters the composition of cells in SVF isolated from the mammary adipose tissues. Adiponectin-deficient SVF contribute to the metaplastic features of the basal epithelial-like breast cancers. Co-implantation of SVF derived from adiponectin-deficient mice accelerates mammary tumor development and metastasis in NOD/SCID mice engrafted with MDA-MB-231 human breast cancer cells. Fluorescence Activated Cell Sorting isolates a population of CD44+CD25-CD100+ cells that are enriched in both thymus and SVF of mice lacking the expression of adiponectin. Upregulated CD100 expression interrupts early T-cell development and maturation. In mammary tissues, CD44+CD25-CD100+ cells facilitate the development of metaplastic basal epithelial-like breast cancers. Adiponectin treatment down-regulates CD100 expression, in turn enhancing Notch signaling and T-cell maturation in the thymus, and reduces the accumulation of CD44+CD25-CD100+ cells in the tumor microenvironment. CONCLUSIONS: These results support a pivotal role of adiponectin in mediating the epithelial-stroma crosstalk to prevent mammary carcinogenesis and shed new lights on the development of immuno-therapeutics for breast cancer diseases. | - |
dc.language | eng | - |
dc.publisher | American Society of Clinical Oncology. The Journal's web site is located at http://www.jco.org/ | - |
dc.relation.ispartof | Journal of Clinical Oncology | - |
dc.title | Modulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Wang, Y: yuwanghk@hku.hk | - |
dc.identifier.authority | Wang, Y=rp00239 | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1200/jco.2015.33.28_suppl.34 | - |
dc.identifier.pmid | 28147780 | - |
dc.identifier.hkuros | 265375 | - |
dc.identifier.volume | 33 | - |
dc.identifier.issue | 28 suppl. | - |
dc.identifier.spage | 34 | - |
dc.identifier.epage | 34 | - |
dc.identifier.isi | WOS:000378097000035 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0732-183X | - |