ArticleSignal transduction and targeted therapy2025
A novel peptide 66CTG stabilizes Myc proto-oncogene protein to promote triple-negative breast cancer growth.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Article
- A single-molecule prodrug synergistically suppresses MYC-amplified osteosarcoma through sequential nitric oxide release and photodynamic therapy.Smart molecules : open access · 2026Article
- Targeting non-coding RNAs in the ferroptosis system: Molecular mechanisms and clinical translation for reversing doxorubicin resistance in breast cancer.Non-coding RNA research · 2026Review
- Article
- Stage-Specific Regulation of Ubiquitination Modifications and Prospects for Targeted Therapy in Triple-Negative Breast Cancer.Oncology research · 2026Review
- LncRNAs as regulators of chemoresistance and chemosensitivity in triple-negative breast cancer.Genetics and molecular biology · 2026Article
- Regulatory roles of LncRNAs in colorectal cancer immune evasion: current concepts and future perspectives.Discover oncology · 2025Review
- Micropeptides Encoded by Noncoding RNAs: Biological Functions and Roles in Diseases.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer that lacks reliable targets for diagnosis and therapy. Non-coding RNA (ncRNA)-encoded products hold promise for addressing this unmet need. By analyzing the reported ribosomal RNA sequencing data, combined with the TCGA, ORFfinder, SmProt databases, we identified CDKN2B-AS1, a TNBC-upregulated lncRNA encoding a 66-amino-acid peptide via CUG-initiated translation. CRISPR-Cas9 gene editing and mass spectrometry confirmed endogenous expression of this peptide, designated 66CTG, in TNBC cells. Functionally independently of its host RNA, 66CTG promoted the proliferation of TNBC cells and the tumor growth of TNBC xenograft by stabilizing c-Myc protein and enhancing Cyclin D1 transcription. Immunohistochemistry of 89 clinical TNBC paraffin samples revealed positive correlations among 66CTG, c-Myc, and Cyclin D1 expression levels. Mechanistically, co-immunoprecipitation and ubiquitination assays revealed that 66CTG stabilized c-Myc by competitively interacting with FBW7α, an E3 ligase responsible for recognizing 66CTG CPD
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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.