Mesenchymal transition and dissemination of cancer cells is driven by myeloid-derived suppressor cells infiltrating the primary tumor

  • 0Singapore Immunology Network, BMSI, A-STAR, Singapore.

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Summary

This summary is machine-generated.

Immune cells called myeloid-derived suppressor cells (MDSC) promote early cancer cell metastasis by inducing epithelial-mesenchymal transition (EMT). These findings reveal a faster route to cancer cell motility and link inflammation to cancer progression.

Area Of Science

  • Oncology
  • Immunology
  • Cell Biology

Background

  • Cancer cell metastasis requires a motile phenotype, traditionally thought to arise from late-stage mutations.
  • Recent evidence suggests cancer cells disseminate early, indicating a faster pathway to motility.
  • The link between inflammation and cancer progression is well-established but mechanistically unclear.

Purpose Of The Study

  • To investigate the mechanism behind early cancer cell dissemination and motility.
  • To identify the role of immune cells in promoting cancer cell metastasis.
  • To elucidate the molecular pathways involved in inflammation-induced cancer progression.

Main Methods

  • Utilized a spontaneous murine melanoma model.
  • Investigated the infiltration of myeloid-derived suppressor cells (MDSC) into primary tumors.
  • Conducted in vitro assays with purified MDSC to assess their effect on cancer cells.
  • Analyzed chemokine signaling (CXCL5) and intracellular pathways (TGF-β, EGF, HGF).

Main Results

  • Myeloid-derived suppressor cells (MDSC) preferentially infiltrate primary tumors.
  • MDSC actively induce epithelial-mesenchymal transition (EMT) in cancer cells, promoting motility.
  • CXCL5 is identified as the primary chemokine attracting MDSC to the tumor site.
  • MDSC utilize TGF-β, EGF, and HGF signaling pathways to induce EMT in cancer cells.

Conclusions

  • MDSC play a crucial role in promoting early cancer cell metastasis by inducing EMT.
  • CXCL5-mediated MDSC recruitment is a key step in facilitating cancer cell dissemination.
  • The study provides a mechanistic link between inflammation and cancer progression via MDSC-induced EMT.
  • Findings offer potential therapeutic targets for preventing cancer metastasis.

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