CXCL17-derived CD11b+Gr-1+ myeloid-derived suppressor cells contribute to lung metastasis of breast cancer through platelet-derived growth factor-BB.

Background: Metastasis is the major cause of death from breast cancer. Colonization and adaption of metastatic cells in distant organs is a rate-limiting step of the cancer spreading. The underlying mechanisms responsible for the colonization of breast cancer to lung metastatic niches are not fully...

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Published in:Breast Cancer Research Vol. 21; no. 1
Main Authors: Hsu, Ya-Ling, Yen, Meng-Chi, Chang, Wei-An, Tsai, Pei-Hsun, Pan, Yi-Chung, Liao, Ssu-Hui, Kuo, Po-Lin
Format: research Journal Article
Published: BioMed Central 2/12/2019
Online Access:View this record in EBSCOhost
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        14655411
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      jtl: Breast Cancer Research
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      dt: 2/12/2019
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      pub: BioMed Central
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        10.1186/s13058-019-1114-3
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        atl: CXCL17-derived CD11b+Gr-1+ myeloid-derived suppressor cells contribute to lung metastasis of breast cancer through platelet-derived growth factor-BB.
      aug:
        au:
          Hsu, Ya-Ling
          Yen, Meng-Chi
          Chang, Wei-An
          Tsai, Pei-Hsun
          Pan, Yi-Chung
          Liao, Ssu-Hui
          Kuo, Po-Lin
        affil: Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, 807, Kaohsiung, Taiwan
      sug:
        subj:
          Chemokines Metabolism
          Breast Neoplasms Pathology
          Lung Neoplasms Pathology
          Cytokines Metabolism
          Kaplan-Meier Estimator
          Human
          Breast Neoplasms Blood
          Receptors, Cell Surface Metabolism
          Animal Studies
          Prognosis
          Cell Physiology
          Breast Neoplasms Mortality
          Female
          Chemokines Blood
          Data Collection
          Lung Pathology
          Cell Line, Tumor
          Mice
          Breast Neoplasms Immunology
          Lung Neoplasms
          Validation Studies
          Comparative Studies
          Evaluation Research
          Multicenter Studies
          Female
      ab: Background: Metastasis is the major cause of death from breast cancer. Colonization and adaption of metastatic cells in distant organs is a rate-limiting step of the cancer spreading. The underlying mechanisms responsible for the colonization of breast cancer to lung metastatic niches are not fully understood.Methods: Specific gene contributions to lung metastasis were identified by comparing gene profiles of 4T1 tumors metastasizing to various organs via microarray. The oncogenic properties CXCL17 were examined by in vivo spontaneous metastasis mouse model. The chemotactic activity of CXCL17 on CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) was examined by both in vitro and in vivo models. The therapeutic effects of MDSC depletion and platelet-derived growth factor-BB (PDGF-BB) inhibition were examined by orthotic models.Results: Here, we demonstrate that breast cancer cells secrete CXCL17, which increases the accumulation of CD11b+Gr-1+ MDSCs in the lungs. Metastatic lung-infiltrating CD11b+Gr-1+ MDSCs induce angiogenesis in the lungs and facilitate cancer extravasation and survival that ultimately promote lung metastases. CXCL17 increases CD11b+Gr-1+ MDSCs to express PDGF-BB, which not only contributes to CD11b+Gr-1+ MDSC-mediated angiogenesis in the lung metastatic niche, but is also involved in the colonization of breast cancer. Consequently, both CD11b+Gr-1+ MDSC depletion and PDGF receptor inhibitor effectively prevents CXCL17-driven lung metastasis in breast cancer. More importantly, patients with high levels of CXCL17 have shorter distant metastasis-free and overall survival rates, indicators of poor prognosis.Conclusion: Our study reveals that MDSCs derived by CXCL17 contribute to the establishment of a lung metastatic niche by PDGF-BB secretion and provide a rationale for development of CXCL17 or PDGF-BB antagonists to inhibit or prevent lung metastasis in cases of breast cancer.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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