ArticleResearch (Washington, D.C.)2024
POP1 Facilitates Proliferation in Triple-Negative Breast Cancer via m6A-Dependent Degradation of CDKN1A mRNA.
Article in Research (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Review
- Review
- mClinical and translational medicine · 2026Article
- Single-cell RNA sequencing reveals immune microenvironment heterogeneity in BRCA1-mutated and sporadic triple-negative breast cancer.Translational oncology · 2026Article
- Deficiency of the mCellular and molecular life sciences : CMLS · 2026Article
- Inhibitory effect of blestriarene C on triple-negative breast cancer: Inducing ferroptosis and mitophagy via SESN2/AKT/FOXO4 axis.Chinese medical journal · 2026Article
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- A novel peptide MIB1-223aa encoded by exosomal circMIB1 from cancer-associated fibroblasts drives triple-negative breast cancer metastasis and stemness via stabilizing MIB1 to activate Notch signaling.Journal of advanced research · 2026Article
- Endocrine Resistance Score Based on Three Key Genes Predicts Prognosis and Reveals Potential Therapeutic Targets for ER+HER2- Breast Cancer.Cell proliferation · 2026Article
- METTL3-mediated mTranslational psychiatry · 2026Article
- EGCG promotes apoptosis in BT-549 triple-negative breast cancer cells by targeting STAT3.Translational cancer research · 2026Article
- Dual-Pronged Lipid Nanocarriers Promote Immunotherapy for TNBC by Inducing Immunogenic Cell Death and Activating Lymphoid Immune Cells.Research (Washington, D.C.) · 2026Article
- Mapping Non-Coding Epimutations in Breast Cancer: Advancing Epigenetics Towards Precision Medicine.Sub-cellular biochemistry · 2026Review
- Destabilization of hsa_circ_0015508 by YTHDF2 Enhances miR-496-Mediated FOXN3 Suppression to Drive Nasopharyngeal Carcinoma Progression.Oncology research · 2026Article
- Transcriptomic Association of COL3A1Pain research & management · 2026Article
- 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
- Ubiquitin D Promotes Lung Metastasis by Stabilizing MMP3 in Triple-Negative Breast Cancer.Research (Washington, D.C.) · 2026Article
- CD44v5 enhances the IL-4/IL-4Rα/STAT6/SAM68 aix inducing M2 polarization and promoting triple-negative breast cancer progression.Cancer biology & therapy · 2025Article
- Co-targeting ferroptosis and immune evasion through small molecules in breast cancer.Journal of translational internal medicine · 2025Article
- ATP6V0D2 drives triple-negative breast cancer progression and inhibits cisplatin sensitivity by promoting PHLPP2 lysosomal degradation.iScience · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Triple-negative breast cancer (TNBC) is currently the worst prognostic subtype of breast cancer, and there is no effective treatment other than chemotherapy. Processing of precursors 1 (POP1) is the most substantially up-regulated RNA-binding protein (RBP) in TNBC. However, the role of POP1 in TNBC remains clarified. A series of molecular biological experiments in vitro and in vivo and clinical correlation analyses were conducted to clarify the biological function and regulatory mechanism of POP1 in TNBC. Here, we identified that POP1 is significantly up-regulated in TNBC and associated with poor prognosis. We further demonstrate that POP1 promotes the cell cycle and proliferation of TNBC in vitro and vivo. Mechanistically, POP1 directly binds to the coding sequence (CDS) region of CDKN1A mRNA and degrades it. The degradation process depends on the N6-methyladenosine (m6A) modification at the 497th site of CDKN1A and the recognition of this modification by YTH N6-methyladenosine RNA binding protein 2 (YTHDF2). Moreover, the m6A inhibitor STM2457 potently impaired the proliferation of POP1-overexpressed TNBC cells and improved the sensitivity to paclitaxel. In summary, our findings reveal the pivotal role of POP1 in promoting TNBC proliferation by degrading the mRNA of CDKN1A and that inhibition of m6A with STM2457 is a promising therapeutic strategy for TNBC.
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