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Updated: Jun 22, 2025

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TWEAK/Fn14 signalling driven super-enhancer reprogramming promotes pro-metastatic metabolic rewiring in

Nicholas Sim1, Jean-Michel Carter1, Kamalakshi Deka1

  • 1School of Biological Sciences (SBS), Nanyang Technological University (NTU), 60 Nanyang Drive, Singapore, 637551, Singapore.

Nature Communications
|July 4, 2024
PubMed

Insights

Fibroblast growth factor-inducible 14 (Fn14) receptor is overexpressed in Triple Negative Breast Cancer (TNBC), driving tumor growth and metastasis. Targeting Fn14 signaling may offer new therapeutic strategies for TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple Negative Breast Cancer (TNBC) is an aggressive subtype with limited treatment options.
  • Fibroblast growth factor-inducible 14 (Fn14) receptor overexpression is linked to metastasis in Estrogen Receptor (ER)-negative breast cancers.

Purpose of the Study:

  • To investigate the role of Fn14 in TNBC.
  • To elucidate the mechanisms by which Fn14 signaling contributes to TNBC progression and metastasis.
  • To identify potential therapeutic targets in TNBC.

Main Methods:

  • Analysis of Fn14 expression in TNBC patients.
  • Transcriptomic and epigenomic profiling of TNBC cells.
  • Investigation of super enhancer (SE) activity and chromatin looping.
  • Assessment of Nicotinamide phosphoribosyltransferase (NAMPT) regulation.

Main Results:

  • Fn14 is overexpressed in TNBC and associated with poor survival.
  • Fn14 signaling alters the transcriptomic and epigenomic landscape, promoting tumor growth and metastasis.
  • SEs drive upregulation of NAMPT, critical for NAD+/ATP metabolism and metastasis.

Conclusions:

  • TWEAK/Fn14 signaling is mechanistically linked to TNBC metastasis.
  • Targeting Fn14 and its downstream pathways presents potential therapeutic vulnerabilities for TNBC.

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