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Updated: Aug 7, 2025

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Published on: October 27, 2014
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.
Objective:
Triple-negative breast cancer (TNBC) is a subtype with high invasiveness. Due to lacking specific and effective therapies, it is necessary to explore the mechanism of TNBC progression and search for new therapeutic targets.
Methods:
Data from the GEPIA2 database was analyzed to explore RNF43 expression in each subtype of breast cancer. RNF43 expression in TNBC tissue and cell lines was determined by RT-qPCR. In vitro biological function analyses including MTT assay, colony formation assay, wound-healing assay and Transwell assay were conducted to explore the role of RNF43 in TNBC. In addition, the markers of epithelial-mesenchymal transition (EMT) were detected by western blot. The expression of β-Catenin and its downstream effectors were also detected.
Results:
Data from the GEPIA2 database indicated that RNF43 expression was lower in tumor tissue compared to paired adjacent tissue in TNBC. In addition, RNF43 expression in TNBC was lower than in other subtypes of breast cancer. Consistently, down-regulation of RNF43 expression in TNBC tissue and cell lines was observed. Overexpressing RNF43 attenuated the proliferation and migration of TNBC cells. Depletion of RNF43 showed the opposite effect, confirming that RNF43 played an anti-oncogenic role in TNBC. In addition, RNF43 suppressed several markers of EMT. Furthermore, RNF43 restrained the expression of β-Catenin and its downstream effectors, implying RNF43 exerted the suppressive role in TNBC by inhibiting the β-Catenin pathway.
Conclusions:
This study demonstrated that the RNF43-β-Catenin axis attenuated TNBC progression, which might provide novel therapeutic targets for TNBC.
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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