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Conference Paper: Modulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment

TitleModulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment
Authors
Issue Date2015
PublisherAmerican 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., v. 33 n. suppl. 28S, abstract no. 34 How to Cite?
AbstractBACKGROUND: 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.
DescriptionPoster Session A: Risk Assessment, Prevention, Early Detection, Screening, and Local/Regional Therapy: abstract no. 34
Persistent Identifierhttp://hdl.handle.net/10722/232561
ISSN
2015 Impact Factor: 20.982
2015 SCImago Journal Rankings: 9.204

 

DC FieldValueLanguage
dc.contributor.authorWang, Y-
dc.date.accessioned2016-09-20T05:30:53Z-
dc.date.available2016-09-20T05:30:53Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 Breast Cancer Symposium, San Francisco, CA., 25-27 September 2015., v. 33 n. suppl. 28S, abstract no. 34-
dc.identifier.issn0732-183X-
dc.identifier.urihttp://hdl.handle.net/10722/232561-
dc.descriptionPoster Session A: Risk Assessment, Prevention, Early Detection, Screening, and Local/Regional Therapy: abstract no. 34-
dc.description.abstractBACKGROUND: 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.languageeng-
dc.publisherAmerican Society of Clinical Oncology. The Journal's web site is located at http://www.jco.org/-
dc.relation.ispartofJournal of Clinical Oncology-
dc.titleModulation of breast cancer development in MMTV-PyVT mice by adiponectin: a perspective on tumor microenvironment-
dc.typeConference_Paper-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.hkuros265375-
dc.identifier.volume33-
dc.identifier.issuesuppl. 28S, abstract no. 34-
dc.publisher.placeUnited States-

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