ArticleMolecular oncology2022
WBP2 promotes BTRC mRNA stability to drive migration and invasion in triple-negative breast cancer via NF-κB activation.
Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Novel function of GTPBP2 in promoting hepatocellular carcinoma progression through inhibition of BTRC-mediated KRAS degradation.Cancer cell international · 2026Article
- Macrophage polarization regulated by the βTrCP-NF-κB inflammatory signaling pathway is required for valproic acid's dual role in breast tumor radiosensitivity and normal tissue radioprotection.Frontiers in immunology · 2026Article
- Leveraging Diverse Cell-Death Patterns to Decipher the Interactive Relation of Unfavorable Outcome and Tumor Microenvironment in Breast Cancer.Bioengineering (Basel, Switzerland) · 2025Article
- NUMB attenuates posttraumatic osteoarthritis by inhibiting BTRC and inactivating the NF-κB pathway.Journal of orthopaedic surgery and research · 2024Article
- SOX2 control activation of dormant prostate cancer cells in bone metastases by promoting CCNE2 gene expression.American journal of clinical and experimental urology · 2024Article
- Review
- Exosomal GPT2 derived from triple-negative breast cancer cells promotes metastasis by activating BTRC.Thoracic cancer · 2023Article
- A Comprehensive Analysis Revealing FBXW9 as a Potential Prognostic and Immunological Biomarker in Breast Cancer.International journal of molecular sciences · 2023Article
- RNA atlas and competing endogenous RNA regulation in tissue-derived exosomes from luminal B and triple-negative breast cancer patients.Frontiers in oncology · 2023Article
- WW domain binding protein 2 (WBP2) as an oncogene in breast cancer: mechanisms and therapeutic prospects-a narrative review.Gland surgery · 2022Review
- Data integration and mechanistic modelling for breast cancer biology: Current state and future directions.Current opinion in endocrine and metabolic research · 2022Review
- Review
- SIPL1, Regulated by MAZ, Promotes Tumor Progression and Predicts Poor Survival in Human Triple-Negative Breast Cancer.Frontiers in oncology · 2021Article
- Establishment of Sunitinib-Resistant Xenograft Model of Renal Cell Carcinoma and the Identification of Drug-Resistant Hub Genes and Pathways.Drug design, development and therapy · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
WW-domain-binding protein 2 (WBP2) is an oncogene that drives breast carcinogenesis through regulating Wnt, estrogen receptor (ER), and Hippo signaling. Recent studies have identified neoteric modes of action of WBP2 other than its widely recognized function as a transcriptional coactivator. Here, we identified a previously unexplored role of WBP2 in inflammatory signaling in breast cancer via an integrated proteogenomic analysis of The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA BRCA) dataset. WBP2 was shown to enhance the migration and invasion in triple-negative breast cancer (TNBC) cells especially under tumor necrosis factor alpha (TNF-α) stimulation. Molecularly, WBP2 potentiates TNF-α-induced nuclear factor kappa B (NF-κB) transcriptional activity and nuclear localization through aggrandizing ubiquitin-mediated proteasomal degradation of its upstream inhibitor, NF-κB inhibitor alpha (NFKBIA; also known as IκBα). We further demonstrate that WBP2 induces mRNA stability of beta-transducin repeat-containing E3 ubiquitin protein ligase (BTRC), which targets IκBα for ubiquitination and degradation. Disruption of IκBα rescued the impaired migratory and invasive phenotypes in WBP2-silenced cells, while loss of BTRC ameliorated WBP2-driven migration and invasion. Clinically, the WBP2-BTRC-IκBα signaling axis correlates with poorer prognosis in breast cancer patients. Our findings reveal a pivotal mechanism of WBP2 in modulating BTRC-IκBα-NF-κB pathway to promote TNBC aggressiveness.
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