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Published on: October 27, 2020

IFITM3 promotes triple-negative breast cancer progression by regulating β-catenin localization

Heeyeon Kim1, Youngim Yu1, Yuseon Park1

  • 1Department of Biological Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.

Biochemical and Biophysical Research Communications
|July 24, 2026
PubMed

Insights

Interferon-induced transmembrane protein 3 (IFITM3) promotes triple-negative breast cancer (TNBC) growth by regulating beta-catenin localization and Wnt signaling. IFITM3 depletion suppressed tumor progression and stem-like properties, indicating its pro-tumorigenic role in TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Interferon-induced transmembrane protein 3 (IFITM3) is recognized for its antiviral properties.
  • Emerging evidence suggests IFITM3 has pro-tumorigenic roles in various cancers.
  • Its specific function in triple-negative breast cancer (TNBC) remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of IFITM3 in the progression of triple-negative breast cancer (TNBC).
  • To determine IFITM3's impact on cell proliferation, migration, stem-like properties, and Wnt/β-catenin signaling in TNBC.
  • To assess the correlation between IFITM3 expression and patient survival in TNBC.

Main Methods:

  • Utilized cell culture models (MDA-MB-231) with IFITM3 depletion and overexpression.
  • Assessed cell proliferation, migration, and sphere formation assays.
  • Analyzed E-cadherin and β-catenin expression and localization.
  • Investigated Wnt/β-catenin transcriptional activity and xenograft tumor growth in vivo.
  • Correlated IFITM3 expression with survival data in a TNBC patient cohort.

Main Results:

  • IFITM3 depletion suppressed TNBC cell proliferation, migration, sphere formation, and xenograft tumor growth.
  • IFITM3 overexpression enhanced these pro-tumorigenic phenotypes.
  • IFITM3 modulated E-cadherin and β-catenin localization, reducing nuclear active β-catenin and Wnt/β-catenin signaling.
  • Conversely, IFITM3 overexpression boosted Wnt signaling.
  • Elevated IFITM3 expression in breast tumors correlated with shorter survival in lymph-node-negative TNBC patients.

Conclusions:

  • IFITM3 acts as a pro-tumorigenic factor in triple-negative breast cancer.
  • IFITM3 regulates β-catenin localization and Wnt signaling pathways.
  • IFITM3 promotes epithelial-mesenchymal transition (EMT) and stem-like characteristics in TNBC.
  • IFITM3 is a potential therapeutic target for TNBC.
Keywords:
E-cadherinEpithelial-mesenchymal transitionIFITM3Triple-negative breast cancerWnt signalingβ-catenin

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