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Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Signaling

Background:

  • Squamous cell carcinomas develop from benign papillomas, driven by RAS-MAPK signaling.
  • Cancer stem cells (CSCs) at tumor interfaces gain resistance to therapies.
  • The role of CSCs in the progression from benign to invasive squamous cell carcinoma is not fully understood.

Purpose of the Study:

  • To investigate the role and mechanisms of cancer stem cells in driving squamous cell carcinoma progression.
  • To elucidate the dynamic signaling crosstalk between CSCs and their microenvironment during malignant transformation.

Main Methods:

  • Utilized a clonal skin HRASG12V mouse model.
  • Employed single-cell transcriptomics, chromatin landscaping, lentiviral reporters, and lineage tracing.
  • Functionally examined key signaling pathways involved in CSC-microenvironment interactions.

Main Results:

  • Oncogenic RAS activation in CSCs triggers gene expression rewiring and aberrant signaling crosstalk.
  • This crosstalk activates angiogenesis, TGFβ, leptin/leptin receptor, and PI3K-AKT-mTOR signaling pathways.
  • Dynamic temporal interactions between CSCs and the microenvironment are critical for malignant progression.

Conclusions:

  • Aberrant, non-genetic intercellular exchanges orchestrated by CSCs fuel the transition to invasive squamous cell carcinoma.
  • Understanding this dynamic crosstalk offers potential therapeutic targets for advanced cancers.
  • Insights into CSC-microenvironment interactions have broad implications for cancer therapeutics.