ArticleCell death and differentiation2018
Enhanced breast cancer progression by mutant p53 is inhibited by the circular RNA circ-Ccnb1.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.
- The Regulation Network and Clinical Significance of Circular RNAs in Breast Cancer.Frontiers in oncology · 2021Pooled it
- Circ_0001495 promotes bladder cancer progression by regulating miR-1184 via MAPK signaling pathway.Molecular biology reports · 2026Article
- Circular RNAs in Intestinal Mucosal Homeostasis and Pathologies.Non-coding RNA · 2026Review
- Circular RNAs: An Under-Recognized Part in Different Scenarios of Host-Parasite Interrelationships.Pathogens (Basel, Switzerland) · 2026Review
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- The impact of p53 mutation on tumor immune evasion: mechanistic insights and clinical implications.Frontiers in immunology · 2026Review
- Circular RNAs orchestrating breast cancer hallmarks: bridging tumor biology and therapy resistance.Functional & integrative genomics · 2025Review
- Plasma Circular RNAs in Breast Cancer: From Biomarker Potential to Functional Significance.Cancer reports (Hoboken, N.J.) · 2025Review
- Multi-omics insights into the roles of CCNB1, PLK1, and HPSE in breast cancer progression: implications for prognosis and immunotherapy.Discover oncology · 2025Article
- CircRNAs: a novel potential strategy to treat breast cancer.Frontiers in immunology · 2025Review
- The ncRNA-AURKA Interaction in Hepatocellular Carcinoma: Insights into Oncogenic Pathways, Therapeutic Opportunities, and Future Challenges.Life (Basel, Switzerland) · 2024Review
- Ferroptosis as a promising targeted therapy for triple negative breast cancer.Breast cancer research and treatment · 2024Review
- Back to the Origin: Mechanisms of circRNA-Directed Regulation of Host Genes in Human Disease.Non-coding RNA · 2024Review
- Circular RNAs in human diseases.MedComm · 2024Review
- Exploring the impact of circRNAs on cancer glycolysis: Insights into tumor progression and therapeutic strategies.Non-coding RNA research · 2024Review
- Circular RNA in cancer.Nature reviews. Cancer · 2024Review
- Advanced approaches of the use of circRNAs as a replacement for cancer therapy.Non-coding RNA research · 2024Review
- Engineering circular RNA for molecular and metabolic reprogramming.Functional & integrative genomics · 2024Review
- Expanding roles of circRNAs in cardiovascular diseases.Non-coding RNA research · 2024Review
- Molecular mechanisms of circular RNA in breast cancer: a narrative review.Translational cancer research · 2024Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
Abstract
TP53 mutations occur in many different types of cancers that produce mutant p53 proteins. The mutant p53 proteins have lost wild-type p53 activity and gained new functions that contribute to malignant tumor progression. Different p53 mutations create distinct profiles in loss of wild-type p53 activity and gain of functions. Targeting the consequences generated by the great number of p53 mutations would be extremely complex. Therefore, in this study we used a workaround and took advantage of the fact that mutant p53 cannot bind H2AX. Using this, we developed a new approach to repress the acquisition of mutant p53 functions. We show here that the delivery of a circular RNA circ-Ccnb1 inhibited the function of three p53 mutations. By microarray analysis and real-time PCR, we detected decreased circ-Ccnb1 expression levels in patients bearing breast carcinoma. Ectopic delivery of circ-Ccnb1 inhibited tumor growth and extended mouse viability. Using proteomics, we found that circ-Ccnb1 precipitated p53 in p53 wild-type cells, but instead precipitated Bclaf1 in p53 mutant cells. Further experiments showed that H2AX serves as a bridge, linking the interaction of circ-Ccnb1 and wild-type p53, thus allowing Bclaf1 to bind Bcl2 resulting in cell survival. In the p53 mutant cells, circ-Ccnb1 formed a complex with H2AX and Bclaf1, resulting in the induction of cell death. We found that this occurred in three p53 mutations. These results shed light on the possible development of new approaches to inhibit the malignancy of p53 mutations.
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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.