RNF43 Suppressed Triple-Negative Breast Cancer Progression by Inhibiting Wnt/beta-Catenin Pathway

Linbo Zhu1, Hong Shi2, Pengfei Li3

  • 1Department of Thyroid and Breast Surgery, Beilun People's Hospital, Ningbo, Zhejiang, China 1711096@tongji.edu.cn.

Abstract

Insights

RNF43 acts as a tumor suppressor in triple-negative breast cancer (TNBC). Its downregulation promotes TNBC progression by activating the β-Catenin pathway, suggesting RNF43 as a potential therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is highly invasive with limited therapeutic options.
  • Understanding TNBC progression mechanisms is crucial for identifying new treatment targets.

Purpose of the Study:

  • To investigate the role of RNF43 in TNBC progression.
  • To explore RNF43 as a potential therapeutic target for TNBC.

Main Methods:

  • Analyzed RNF43 expression in breast cancer subtypes using GEPIA2 database.
  • Assessed RNF43 expression in TNBC tissues and cell lines via RT-qPCR.
  • Performed in vitro functional assays (MTT, colony formation, wound healing, Transwell) and western blot analysis for EMT markers and β-Catenin pathway components.

Main Results:

  • RNF43 expression is downregulated in TNBC tumor tissues and cell lines compared to normal tissues and other breast cancer subtypes.
  • Overexpression of RNF43 inhibited TNBC cell proliferation and migration, while RNF43 depletion enhanced these processes.
  • RNF43 suppressed epithelial-mesenchymal transition (EMT) markers and inhibited the β-Catenin signaling pathway.

Conclusions:

  • The RNF43-β-Catenin axis plays a significant role in attenuating TNBC progression.
  • RNF43 acts as an anti-oncogenic factor in TNBC, highlighting its potential as a novel therapeutic target.

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