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F11 Receptor/Junctional Adhesion Molecule-A: a novel therapeutic target in breast cancer

Radosław Bednarek1, Maria Świątkowska1

  • 1Department of Cytobiology and Proteomics, Chair of Biomedical Sciences, Medical University of Lodz, ul. Mazowiecka 6/8, 92-215, Lodz, Poland.

Biochimie
|August 6, 2026
PubMed

Insights

Junctional adhesion molecule-A (F11R/JAM-A) is a promising therapeutic target for breast cancer (BC). Targeting F11R/JAM-A with peptide antagonists may offer new treatment strategies for BC, including triple-negative breast cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer (BC) is a leading cause of cancer death globally, with metastasis and therapy resistance posing significant challenges.
  • Triple-negative breast cancer (TNBC) lacks specific cell surface markers, limiting treatment options to chemotherapy.
  • Cancer cell metastasis involves disrupting endothelial tight junctions (TJs) and forming new junctions with endothelial cells.

Purpose of the Study:

  • To identify novel molecular targets for breast cancer therapy.
  • To characterize the role of junctional adhesion molecule-A (F11R/JAM-A) in breast cancer progression and metastasis.
  • To evaluate F11R/JAM-A as a potential therapeutic target for breast cancer treatment.

Main Methods:

  • Review of existing literature on breast cancer, metastasis, tight junctions, and F11R/JAM-A.
  • Analysis of studies investigating the role of miR-145 in regulating F11R/JAM-A levels and cell migration in BC.
  • Examination of F11R/JAM-A expression patterns in various cancer types, particularly BC.

Main Results:

  • F11R/JAM-A, a tight junction protein, is frequently overexpressed in breast cancer.
  • Overexpression of miR-145 in BC cells leads to reduced F11R/JAM-A levels and decreased cell migration.
  • F11R/JAM-A plays a critical role in cancer cell migration and metastasis by disrupting endothelial barriers.

Conclusions:

  • F11R/JAM-A is a key mediator of breast cancer progression and metastasis.
  • F11R/JAM-A represents a promising molecular target for developing novel breast cancer therapies.
  • Peptide antagonists targeting F11R/JAM-A show potential as effective anticancer drugs for breast cancer treatment.
Keywords:
Breast cancerEndotheliumMetastasisTargeted therapyTight junctions

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