Macrophage-Secreted S100A4 Supports Breast Cancer Metastasis by Remodeling the Extracellular Matrix in the Premetastatic Niche.

Metastasis is the major cause of cancer-related mortalities. A tumor-supportive microenvironment, also known as the premetastatic niche at secondary tumor sites, plays a crucial role in metastasis. Remodeling of the extracellular matrix (ECM) is essential for premetastatic niche formation, especiall...

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Publicado en:BioMed Research International pp. 1 - 15
Autores principales: Qi, Yana, Zhao, Tingting, Li, Ranran, Han, Mingyong
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 4/20/2022
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 4/20/2022
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2022/9895504
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        atl: Macrophage-Secreted S100A4 Supports Breast Cancer Metastasis by Remodeling the Extracellular Matrix in the Premetastatic Niche.
      aug:
        au:
          Qi, Yana
          Zhao, Tingting
          Li, Ranran
          Han, Mingyong
        affil: Cancer Therapy and Research Center, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021 Shandong, China
      sug:
        subj:
          Breast Neoplasms
          Neoplasm Metastasis
          Extracellular Space
          Animal Studies
          Mice
          Female
          Cell Line, Tumor
          Fibroblasts
          Descriptive Statistics
          Signal Transduction
          Female
      ab: Metastasis is the major cause of cancer-related mortalities. A tumor-supportive microenvironment, also known as the premetastatic niche at secondary tumor sites, plays a crucial role in metastasis. Remodeling of the extracellular matrix (ECM) is essential for premetastatic niche formation, especially for circulating tumor cell colonization. However, the underlying molecular mechanism that contributes to this effect remains unclear. Here, we developed a lung metastasis model with 4T1 breast cancer cells and found that the metastasis critically depended on the early recruitment of macrophages to the lung. Disruption of macrophage recruitment reduced fibroblast activation and lung metastasis. Furthermore, we identified the secreted protein S100A4, which is produced by M2 macrophages and participates in fibroblast activation and ECM protein deposition via the ERK signaling pathway. Collectively, these results indicate that recruiting S100A4-expressing inflammatory macrophages plays a vital role in ECM remodeling in the premetastatic niche and may act as a potential therapeutic target for breast cancer lung metastasis.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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