Cited by 925TGF-β signaling in diseasesImmune cells in cancerChemokine receptors and signaling

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Abrogation of TGFβ Signaling in Mammary Carcinomas Recruits Gr-1+CD11b+ Myeloid Cells that Promote Metastasis

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Yang, Li, Huang, Jianhua, Ren, Xiubao, Gorska, Agnieszka E., Chytil, Anna, Aakre, Mary, Carbone, David P., Matrisian, Lynn M., Richmond, Ann, Lin, P. Charles, Moses, Harold L.·2008·Cancer Cell

DOI 10.1016/j.ccr.2007.12.004PMC PMC2245859

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Abstract

Aberrant TGFbeta signaling is common in human cancers and contributes to tumor metastasis. Here, we demonstrate that Gr-1+CD11b+ myeloid cells are recruited into mammary carcinomas with type II TGF beta receptor gene (Tgfbr2) deletion and directly promote tumor metastasis. Gr-1+CD11b+ cells infiltrate into the invasive front of tumor tissues and facilitate tumor cell invasion and metastasis through a process involving metalloproteinase activity. This infiltration of Gr-1+CD11b+ cells also results in increased abundance of TGF beta 1 in tumors with Tgfbr2 deletion. The recruitment of Gr-1+CD11b+ cells into tumors with Tgfbr2 deletion involves two chemokine receptor axes, the SDF-1/CXCR4 and CXCL5/CXCR2 axes. Together, these data indicate that Gr-1+CD11b+ cells contribute to TGFbeta-mediated metastasis through enhancing tumor cell invasion and metastasis.

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Self-citation
Enzymatic Inactivation of Oxysterols in Breast Tumor Cells Constraints Metastasis Formation by Reprogramming the Metastatic Lung Microenvironment
Moresco, M. A., Raccosta, L., Corna, G., Maggioni, D., Soncini, M., Bicciato, S., Doglioni, C., & Russo, V. E. A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02251 · Cited by 24

Authors: Yang, L., Huang, J., Ren, X., Gorska, A. E., Chytil, A., Aakre, M., Carbone, D. P., Matrisian, L. M., Richmond, A., Lin, P. C., & Moses, H. L.
Affiliations: Vanderbilt University (US)
Corresponding author: Moses, Harold L.
ORCID: Huang, Jianhua
Ren, Xiubao
Gorska, Agnieszka E.
Carbone, David P.
Matrisian, Lynn M.
Richmond, Ann
Moses, Harold L.
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2008-01
Volume: 13
Issue: 1
Pages: 23-35
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccr.2007.12.004
PMC: PMC2245859
OpenAlex: W2130870648
Cited by: 918
References: 61
Citations by year: 2026: 10 · 2025: 19 · 2024: 30 · 2023: 25 · 2022: 41 · 2021: 58 · 2020: 41 · 2019: 52 · 2018: 42 · 2017: 47 · 2016: 62 · 2015: 59 · 2014: 64 · 2013: 78 · 2012: 77
FWCI: 29.18
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 2024 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: U.S. Department of Veterans Affairs (IK6 BX005225)
Vanderbilt University
National Cancer Institute (CA068485, CA 085492, R01CA085492, R01CA116021, CA102162, R01CA108856, CA126505, R01CA076321, R01CA034590, P50CA098131, R01CA102162, CA108856, P30CA068485, U54CA126505)
National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK58404, P30DK058404)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords: TGF-beta signaling, breast cancer, tumor-associated macrophages, metastasis, tumor invasion, metalloproteinase activity, SDF-1/CXCR4 axis, chemokine receptors, myeloid cell recruitment
MeSH terms: Receptor, Transforming Growth Factor-beta Type II, Animals, Breast Neoplasms, Female, Humans, Models, Biological, Neoplasm Invasiveness, Neoplasm Metastasis, Signal Transduction, Transforming Growth Factor beta, Protein Serine-Threonine Kinases, Gene Deletion, Receptors, Transforming Growth Factor beta, Matrix Metalloproteinases, Myeloid Cells, CD11b Antigen, Cell Line, Tumor, Mice

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Abrogation of TGFβ Signaling in Mammary Carcinomas Recruits Gr-1+CD11b+ Myeloid Cells that Promote Metastasis

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