TMEM205 promotes M2-like macrophage polarization and advances the progression of triple-negative breast cancer

Yining Zhang1, Jing Peng1, Teng Ma1

  • 1Breast Disease Center, the Affiliated Hospital of Qingdao University, Qingdao, 266000, Shandong, China.

PubMed
Abstract

Insights

Transmembrane protein 205 (TMEM205) drives triple-negative breast cancer (TNBC) progression by promoting cell growth, metastasis, and angiogenesis. It also creates an immunosuppressive tumor microenvironment, suggesting TMEM205 as a potential therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapy options.
  • The role of transmembrane protein 205 (TMEM205) in TNBC progression and immune evasion is not well understood.

Purpose of the Study:

  • To investigate the function and mechanism of TMEM205 in TNBC.
  • To assess TMEM205's impact on the tumor immune microenvironment.

Main Methods:

  • Analyzed TMEM205 expression and prognostic value using TCGA and UALCAN datasets.
  • Performed in vitro functional assays (CCK-8, colony formation, wound healing, Transwell) in TNBC cell lines with TMEM205 overexpression/knockdown.
  • Utilized coculture systems, Western blot, ELISA, and xenograft mouse models to study tumor-macrophage interactions, signaling pathways, and tumor growth.

Main Results:

  • TMEM205 is upregulated in breast cancer and linked to poor prognosis.
  • TMEM205 overexpression enhances TNBC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
  • TMEM205 upregulates IL-6, activates JAK2/STAT3 signaling, correlates with M2 macrophage infiltration, and promotes angiogenesis.

Conclusions:

  • TMEM205 promotes TNBC progression through proliferation, metastasis, angiogenesis, and immune suppression via M2 macrophage polarization.
  • TMEM205 represents a potential therapeutic target for triple-negative breast cancer.

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