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  • *Cell Transformation, Neoplastic  (1)
  • Breast Cancer Special Feature  (1)
  • Carcinoma, Squamous Cell/etiology/metabolism/pathology  (1)
  • Epithelial Cells/*physiology  (1)
  • Mice, Knockout  (1)
  • 1
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    TGF-beta signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: Stromal cells can have a significant impact on the carcinogenic process in adjacent epithelia. The role of transforming growth factor-beta (TGF-beta) signaling in such epithelial-mesenchymal interactions was determined by conditional inactivation of the TGF-beta type II receptor gene in mouse fibroblasts (Tgfbr2fspKO). The loss of TGF-beta responsiveness in fibroblasts resulted in intraepithelial neoplasia in prostate and invasive squamous cell carcinoma of the forestomach, both associated with an increased abundance of stromal cells. Activation of paracrine hepatocyte growth factor (HGF) signaling was identified as one possible mechanism for stimulation of epithelial proliferation. Thus, TGF-beta signaling in fibroblasts modulates the growth and oncogenic potential of adjacent epithelia in selected tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhowmick, Neil A -- Chytil, Anna -- Plieth, David -- Gorska, Agnieszka E -- Dumont, Nancy -- Shappell, Scott -- Washington, M Kay -- Neilson, Eric G -- Moses, Harold L -- AR41943/AR/NIAMS NIH HHS/ -- CA102162/CA/NCI NIH HHS/ -- CA68485/CA/NCI NIH HHS/ -- CA85492/CA/NCI NIH HHS/ -- DK46282/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764882" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/etiology/metabolism/pathology ; Cell Division ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Epithelial Cells/*physiology ; Female ; Fibroblasts/*physiology ; Hepatocyte Growth Factor/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Neoplasms, Glandular and Epithelial/*etiology/metabolism/pathology ; Prostate/cytology/metabolism/pathology ; Prostatic Intraepithelial Neoplasia/etiology/metabolism/pathology ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins c-met/metabolism ; Receptors, Transforming Growth Factor beta/genetics/metabolism ; Recombination, Genetic ; *Signal Transduction ; Stomach/cytology/metabolism/pathology ; Stomach Neoplasms/etiology/metabolism/pathology ; Stromal Cells/*physiology ; Transforming Growth Factor beta/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Disruption of bone morphogenetic protein receptor 2 (BMPR2) in mammary tumors promotes metastases through cell autonomous and paracrine mediators [Cell Biology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-02-22
    Description: Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily of signaling molecules. BMPs can elicit a wide range of effects in many cell types and have previously been shown to induce growth inhibition in carcinoma cells as well as normal epithelia. Recently, it has been demonstrated that BMP4 and BMP7 are overexpressed in human breast cancers and may have tumor suppressive and promoting effects. We sought to determine whether disruption of the BMP receptor 2 (BMPR2) would alter mammary tumor progression in mice that express the Polyoma middle T antigen. Mice expressing Polyoma middle T antigen under the mouse mammary tumor virus promoter were combined with mice that have doxycycline-inducible expression of a dominant-negative (DN) BMPR2. We did not observe any differences in tumor latency. However, mice expressing the BMPR2-DN had a fivefold increase in lung metastases. We characterized several cell autonomous changes and found that BMPR2-DN–expressing tumor cells had higher rates of proliferation. We also identified unique changes in inflammatory cells and secreted chemokines/cytokines that accompanied BMPR2-DN–expressing tumors. By immunohistochemistry, it was found that BMPR2-DN primary tumors and metastases had an altered reactive stroma, indicating specific changes in the tumor microenvironment. Among the changes we discovered were increased myeloid derived suppressor cells and the chemokine CCL9. BMP was shown to directly regulate CCL9 expression. We conclude that BMPR2 has tumor-suppressive function in mammary epithelia and microenvironment and that disruption can accelerate mammary carcinoma metastases.
    Keywords: Breast Cancer Special Feature
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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