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RNF114 Interacts with EWSR1 to Regulate VEGFR2 in HER2-positive Breast Cancer
Yingchuan Zhu1, Yue Song1, Yilu Lu1
1Department of Medical Genetics, Frontiers Science Center for Disease-related Molecular Networks, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Journal of Cancer
|March 17, 2025
Summary
RNF114, an E3 ubiquitin ligase, drives tumor growth and autophagy in HER2-positive breast cancer by interacting with EWSR1 and regulating VEGFR2. Its overexpression correlates with poor prognosis, highlighting its oncogenic role.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- RNF114 is an E3 ubiquitin ligase amplified in various cancers.
- Previous research linked RNF114 E3 ligase activity to synthetic lethality in BRCA-mutated cancers.
- Novel functions and interacting molecules of RNF114 require elucidation.
Purpose of the Study:
- To investigate the novel functions of RNF114 in HER2-positive breast cancer (BC).
- To identify interacting molecules and downstream targets of RNF114 in BC.
- To explore the role of RNF114 in tumor proliferation, migration, invasion, and autophagy.
Main Methods:
- Investigated RNF114 interactions with EWSR1 and regulation of VEGFR2 expression.
- Assessed RNF114 expression levels in breast cancer patient cohorts.
- Utilized knockdown experiments to evaluate the functional impact of RNF114 on BC cell behavior.
Main Results:
- RNF114 promotes tumor proliferation and autophagy via EWSR1 interaction and VEGFR2 regulation in HER2-positive BC.
- RNF114 is significantly overexpressed in BC, correlating with advanced TNM stage and poor patient prognosis.
- Knockdown of RNF114 suppressed proliferation, migration, invasion, and autophagy in HER2-positive BC cells.
Conclusions:
- RNF114 possesses a transcriptional regulatory function in breast cancer.
- RNF114 plays a significant oncogenic role in the progression of HER2-positive breast cancer.
- RNF114 represents a potential therapeutic target for HER2-positive breast cancer.
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