ArticleMolecular and cellular biochemistry2025
CircXPO6 promotes breast cancer progression through competitively inhibiting the ubiquitination degradation of c-Myc.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Identification of a prognostic model using immune related genes combined with tumour mutational burden and T cell infiltration in triple-negative breast cancer.Oncology letters · 2026Article
- The effect of pentacyclic triterpene-NIR-AIE derivatives on the proliferation, migration and apoptosis of Melanoma cells.Scientific reports · 2026Article
- Circular and Long Non-Coding RNAs in Cancer Metabolism: Dual Perspective of Biomarkers and Therapeutic Targets.Non-coding RNA · 2026Review
- Regulation of Cell Function and Myeloid-Derived Suppressor Cell Chemotaxis by hsa_circ_0006466-miR-1286-PDGFRA/B Axis in Triple Negative Breast Cancer.Analytical cellular pathology (Amsterdam) · 2026Article
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- Ubiquitination in cancer: mechanisms and therapeutic opportunities.Cancer communications (London, England) · 2025Review
- The Dual Roles of Circular RNAs in Breast Cancer Distant Metastasis and Their Clinical Applications.Journal of Cancer · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The number of breast cancer (BC) patients is increasing year by year, which is severely endangering to human life and health. c-Myc is a transcription factor, studies have shown that it is a very significant factor in tumor progression, but how it is regulated in BC is still not well understood. Here, we used the RIP microarray sequencing to confirm circXPO6, which had a high affinity with c-Myc and highly expressed in triple-negative breast cancer (TNBC) tissues and cells. CircXPO6 overexpression promoted tumor growth in vivo and in vitro. Furthermore, circXPO6 largely promoted the expression of genes related to glucose metabolism, such as GLUT1, HK2, and MCT4 in TNBC cells. Finally, high levels of circXPO6 expression were found to be closely associated with malignant pathological factors, such as tumor size, lymph node metastasis, TNM staging, and histopathological grading of TNBC. Mechanistically, circXPO6 interacted with c-Myc to prevent speckle-type POZ-mediated c-Myc ubiquitination and degradation, thus promoting TNBC progression. Through the regulation of c-Myc-mediated signal transduction, circXPO6 plays a key role in TNBC progresses. This discovery can provide new ideas for TNBC molecular targeted therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.