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CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling

Zhao-Hui Chen1,2,3,4, Yao Tian1,2,3,4,5, Guang-Lei Zhou1,2,3,4

  • 1The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Huan-Hu-Xi Road, He-Xi District, Tianjin, 300060, China.

Breast Cancer Research : BCR
|February 24, 2023
PubMed
Abstract

Insights

Chemokine-like factor MARVEL transmembrane domain containing 7 (CMTM7) acts as a tumor suppressor in breast cancer. A feedback loop involving CMTM7, miR-182-5p, and Wnt/β-catenin signaling influences cancer progression and offers therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer is a leading cause of mortality in women globally.
  • Chemokine-like factor MARVEL transmembrane domain containing 7 (CMTM7) is a known tumor suppressor involved in EGFR degradation and PI3K/AKT signaling.
  • The precise molecular mechanisms of CMTM7 in breast cancer remain incompletely understood.

Purpose of the Study:

  • To elucidate the role and molecular mechanisms of CMTM7 in breast cancer progression.
  • To investigate the regulatory network involving CMTM7, microRNAs, and signaling pathways.
  • To identify potential therapeutic targets for breast cancer based on CMTM7 interactions.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot to assess CMTM7 expression.
  • Bisulfite sequencing PCR (BSP) to analyze CMTM7 promoter methylation.
  • In vitro and in vivo assays (MTT, colony formation, EdU, Transwell, wound healing) to evaluate CMTM7 function.
  • Co-immunoprecipitation (Co-IP) to study CMTM7-CTNNA1 interaction.
  • Luciferase reporter and ChIP assays to determine regulatory relationships involving miR-182-5p and TCF3.

Main Results:

  • Hypermethylation of the CMTM7 promoter was observed in breast cancer tissues and cell lines.
  • CMTM7 exhibited tumor-suppressive effects both in vitro and in vivo.
  • CMTM7 was identified as a direct target of miR-182-5p.
  • CMTM7 interacts with Catenin Alpha 1 (CTNNA1), modulating Wnt/β-catenin signaling.
  • Transcription factor 3 (TCF3) was found to regulate miR-182-5p.
  • A feedback loop comprising miR-182-5p, CMTM7, CTNNA1, CTNNB1 (β-catenin), and TCF3 was identified as crucial for breast cancer progression.

Conclusions:

  • CMTM7 plays a significant role in Wnt/β-catenin signaling and exhibits tumor-suppressive functions in breast cancer.
  • The identified feedback loop involving miR-182-5p, CMTM7, CTNNA1, CTNNB1, and TCF3 offers new insights into gene interactions in breast cancer.
  • CMTM7 and other components of this feedback loop represent potential therapeutic targets for breast cancer treatment.
Keywords:
Breast cancerCMTM7CTNNA1Wnt/β-catenin signalingmiR-182-5p

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