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A Targetable Developmental Program Coregulates Angiogenesis and Immune Evasion in Melanoma.

Pietro Berico1,2, Amanda Flores Yanke1,2, Fatemeh Vand-Rajabpour1,2

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The homeodomain transcription factor HOXD13 drives melanoma growth by promoting blood vessel formation and blocking immune cell entry. Inhibiting its targets reverses these effects, offering new therapeutic strategies for melanoma.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Ultraviolet radiation induces DNA mutations in melanoma, creating neoantigens that can stimulate anti-tumor immunity.
  • Melanoma cells evade immune detection through epigenetic changes and by interacting with their microenvironment.
  • Solid tumors often exhibit increased vascularization that paradoxically limits immune cell infiltration.

Purpose of the Study:

  • To investigate the role of transcription factors in melanoma progression and immune evasion.
  • To identify specific molecular mechanisms driving angiogenesis and immune suppression in melanoma.
  • To explore potential therapeutic targets based on identified molecular pathways.

Main Methods:

  • Comparative analysis of transcription factor expression in melanoma, naevi, and other cancers.
  • Transcriptomic analysis and 3D chromatin profiling.
  • In vivo melanoma models to assess HOXD13 function and therapeutic interventions.

Main Results:

  • HOXD13, a homeodomain transcription factor, drives a melanoblast-like program in melanoma, correlating with angiogenesis and immune exclusion.
  • HOXD13 promotes tumor growth by enhancing angiogenesis and suppressing T-cell infiltration.
  • HOXD13 activates VEGFA, SEMA3A, and CD73 via 3D enhancer-promoter interactions, leading to vascular remodeling and adenosine-mediated immunosuppression.

Conclusions:

  • HOXD13 plays a critical role in melanoma pathogenesis by orchestrating a dual pro-angiogenic and immunosuppressive axis.
  • Combined inhibition of Vascular Endothelial Growth Factor Receptor (VEGFR) and adenosine receptors (AdR) effectively reverses HOXD13-induced tumor growth.
  • Targeting the HOXD13 pathway presents a promising therapeutic strategy for cutaneous melanoma.