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Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast

Can Jiang1, Zhengwei Zhou1, Guang Shu1

  • 1Department of Pathology, Xiangya School of Basic Medical Sciences, Central South University, Changsha 410013, China.

Biology
|November 27, 2025
PubMed

Insights

This study identifies TNFRSF12A as a key gene overexpressed in triple-negative breast cancer (TNBC). TNFRSF12A promotes TNBC progression and enhances docetaxel sensitivity, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies and has a poor prognosis.
  • Novel therapeutic strategies are urgently needed for TNBC.
  • TNBC is defined by the absence of Estrogen Receptor (ER), Progesterone Receptor (PR), and HER2 expression.

Purpose of the Study:

  • To identify key genes driving TNBC progression.
  • To investigate the role of TNFRSF12A in TNBC.
  • To explore TNFRSF12A's impact on the tumor microenvironment and chemoresistance.

Main Methods:

  • Gene expression analysis in TNBC tissues.
  • Functional enrichment analysis (STRING/DAVID).
  • Immune infiltration profiling (TIMER/TISCH2).
  • Molecular docking simulations.
  • Cellular assays (HUVEC tube formation, CCK-8).

Main Results:

  • TNFRSF12A is significantly overexpressed in TNBC and correlates with worse outcomes.
  • TNFRSF12A promotes angiogenesis, cell migration, and hypoxia response.
  • TNFRSF12A is enriched in cancer-associated fibroblasts (CAFs) and inversely correlates with T-cell and B-cell infiltration.
  • Elevated TNFRSF12A enhances sensitivity to docetaxel.
  • TNFRSF12A knockdown impairs angiogenesis, augments T-cell cytotoxicity, and reduces docetaxel sensitivity.

Conclusions:

  • TNFRSF12A drives TNBC progression by modulating the tumor immune microenvironment and promoting angiogenesis.
  • TNFRSF12A plays a crucial role in docetaxel chemoresistance.
  • Targeting TNFRSF12A offers potential for novel combination therapies in TNBC.
Keywords:
TNFRSF12Aangiogenesistriple-negative breast cancertumor immune microenvironment

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