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Cancer-associated fibroblast (CAF) SDC1 drives radioresistance in triple-negative breast cancer (TNBC) by promoting aerobic glycolysis and immune suppression. Targeting SDC1+ CAFs with antibody-drug conjugates synergizes with radiotherapy.

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Area of Science:

  • Oncology
  • Cancer Biology
  • Immunology

Background:

  • Radiotherapy resistance is a significant challenge in treating triple-negative breast cancer (TNBC).
  • Cancer-associated fibroblasts (CAFs) play a crucial role in the tumor microenvironment and can influence treatment response.

Purpose of the Study:

  • To investigate the role of SDC1 in CAF-mediated radioresistance in TNBC.
  • To elucidate the underlying mechanisms by which CAFs confer radioresistance.

Main Methods:

  • Identified SDC1 as a mediator of CAF-induced radioresistance.
  • Investigated the interaction between SDC1 and the glycolytic enzyme ENO1.
  • Assessed the impact of the lactate-rich microenvironment on tumor stemness and immune cells.
  • Evaluated the efficacy of targeting SDC1+ CAFs with indatuximab ravtansine (BT062) in combination with radiotherapy in vivo.

Main Results:

  • SDC1 binds ENO1, preventing its degradation and promoting aerobic glycolysis and lactate accumulation.
  • The resulting lactate-rich environment enhances tumor stemness and suppresses NK and CD8+ T cell functions.
  • Pharmacologic inhibition of ENO1 or lactate export restored radiosensitivity.
  • Targeting SDC1+ CAFs with BT062 synergized with radiotherapy, reducing tumor burden and stem-like cells, and remodeling the immune microenvironment.

Conclusions:

  • SDC1 in CAFs drives TNBC radioresistance through a metabolic program fueling tumor stemness and immune suppression.
  • Targeting SDC1+ CAFs represents a promising therapeutic strategy for TNBC, enhancing radiosensitivity and immune function.