論文

最終著者 国際誌
2019年12月16日

Cancer Cell-Derived Granulocyte-Macrophage Colony-Stimulating Factor Is Dispensable for the Progression of 4T1 Murine Breast Cancer.

International journal of molecular sciences
  • Teizo Yoshimura
  • ,
  • Kaoru Nakamura
  • ,
  • Chunning Li
  • ,
  • Masayoshi Fujisawa
  • ,
  • Tsuyoshi Shiina
  • ,
  • Mayu Imamura
  • ,
  • Tiantian Li
  • ,
  • Naofumi Mukaida
  • ,
  • Akihiro Matsukawa

20
24
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/ijms20246342

We previously reported that 4T1 murine breast cancer cells produce GM-CSF that up-regulates macrophage expression of several cancer promoting genes, including Mcp-1/Ccl2, Ccl17 and Rankl, suggesting a critical role of cancer cell-derived GM-CSF in cancer progression. Here, we attempted to define whether 4T1 cell-derived GM-CSF contributes to the expression of these genes by 4T1tumors, and their subsequent progression. Intraperitoneal injection of anti-GM-CSF neutralizing antibody did not decrease the expression of Mcp-1, Ccl17 or Rankl mRNA by 4T1 tumors. To further examine the role of cancer cell-derived GM-CSF, we generated GM-CSF-deficient 4T1 cells by using the Crisper-Cas9 system. As previously demonstrated, 4T1 cells are a mixture of cells and cloning of cells by itself significantly reduced tumor growth and lung metastasis. By contrast, GM-CSF-deficiency did not affect tumor growth, lung metastasis or the expression of these chemokine and cytokine genes in tumor tissues. By in-situ hybridization, the expression of Mcp-1 mRNA was detected in both F4/80-expressing and non-expressing cells in tumors of GM-CSF-deficient cells. These results indicate that cancer cell-derived GM-CSF is dispensable for the tuning of the 4T1 tumor microenvironment and the production of MCP-1, CCL17 or RANKL in the 4T1 tumor microenvironment is likely regulated by redundant mechanisms.

リンク情報
DOI
https://doi.org/10.3390/ijms20246342
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31888216
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6941073
ID情報
  • DOI : 10.3390/ijms20246342
  • PubMed ID : 31888216
  • PubMed Central 記事ID : PMC6941073

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