ArticleCell death and differentiation2020
Targeting PML in triple negative breast cancer elicits growth suppression and senescence.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 64 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- Precision post-translational modification of PML defines neuroblastoma clinical behaviour.Clinical and translational medicine · 2026Article
- Exploring PIM1 Kinase as a Therapeutic Target: Mechanisms and Strategies in Cancer Treatment.International journal of molecular sciences · 2026Review
- The promyelocytic leukemia PML protein coordinates immune evasion in triple-negative breast cancer via independent and converging mechanisms.Cell death and differentiation · 2026Article
- NAT10-mediated N4-acetylcytidine modification drives RNA splicing of PML to alleviate adipose-derived stem cell senescence and promote diabetic wound healing.Clinical and translational medicine · 2026Article
- HORMAD1 inhibits senescence and promotes proliferation of triple negative breast cancer by facilitating ubiquitination-mediated degradation of p27.American journal of translational research · 2026Article
- A DSSM network for inferring and prioritizing cell-type-specific regulons using single-cell RNA-seq data.BMC bioinformatics · 2025Article
- Regulation of ribosomal gene expression and senescence by a PML-mTOR-RONIN nuclear complex in triple-negative breast cancer.Oncogene · 2025Article
- A bioinformatics screen identifies TCF19 as an aggressiveness-sustaining gene in prostate cancer.Molecular oncology · 2025Article
- Membraneless Organelles and Phase Separation in Tumours: Mechanisms and Prospects.Cell proliferation · 2025Review
- System analysis based on Anoikis-related genes identifies MAPK1 as a novel therapy target for osteosarcoma with neoadjuvant chemotherapy.BMC musculoskeletal disorders · 2024Article
- The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer.Cell death and differentiation · 2024Article
- PML restrains p53 activity and cellular senescence in clear cell renal cell carcinoma.EMBO molecular medicine · 2024Article
- History of Developing Acute Promyelocytic Leukemia Treatment and Role of Promyelocytic Leukemia Bodies.Cancers · 2024Review
- A Novel Cellular Senescence-related lncRNA Signature for Predicting the Prognosis of Breast Cancer Patients.Journal of Cancer · 2024Article
- Curcumin improves atrial fibrillation susceptibility by regulating tsRNA expression in aging mouse atrium.PeerJ · 2024Article
- PML modulates epigenetic composition of chromatin to regulate expression of pro-metastatic genes in triple-negative breast cancer.Nucleic acids research · 2023Article
- Promyelocytic leukemia protein regulates angiogenesis and epithelial-mesenchymal transition to limit metastasis in MDA-MB-231 breast cancer cells.Molecular oncology · 2023Article
- Suppression of Ah Receptor (AhR) increases the aggressiveness of TNBC cells and 11-Cl-BBQ-activated AhR inhibits their growth.Biochemical pharmacology · 2023Article
- Changes in the mammary gland during aging and its links with breast diseases.Acta biochimica et biophysica Sinica · 2023Review
Corrections and comments
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Authors and funding
23 authors at 6 institutions in 2 countries.
Funding
Abstract
Oncogene addiction postulates that the survival and growth of certain tumor cells is dependent upon the activity of one oncogene, despite their multiple genetic and epigenetic abnormalities. This phenomenon provides a foundation for molecular targeted therapy and a rationale for oncogene-based stratification. We have previously reported that the Promyelocytic Leukemia protein (PML) is upregulated in triple negative breast cancer (TNBC) and it regulates cancer-initiating cell function, thus suggesting that this protein can be therapeutically targeted in combination with PML-based stratification. However, the effects of PML perturbation on the bulk of tumor cells remained poorly understood. Here we demonstrate that TNBC cells are addicted to the expression of this nuclear protein. PML inhibition led to a remarkable growth arrest combined with features of senescence in vitro and in vivo. Mechanistically, the growth arrest and senescence were associated to a decrease in MYC and PIM1 kinase levels, with the subsequent accumulation of CDKN1B (p27), a trigger of senescence. In line with this notion, we found that PML is associated to the promoter regions of MYC and PIM1, consistent with their direct correlation in breast cancer specimens. Altogether, our results provide a feasible explanation for the functional similarities of MYC, PIM1, and PML in TNBC and encourage further study of PML targeting strategies for the treatment of this breast cancer subtype.
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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.