ArticlePloS one2013
Targeting the EGFR/PCNA signaling suppresses tumor growth of triple-negative breast cancer cells with cell-penetrating PCNA peptides.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- Review
- Proliferative Markers in Breast Cancer and Chemotherapy Implications: A Comprehensive Review.Health science reports · 2025Article
- Canine mammary tumors as a promising adjunct preclinical model for human breast cancer research: similarities, opportunities, and challenges.Archives of pharmacal research · 2025Review
- Multifaceted impact of HIV inhibitor dapivirine on triple negative breast cancer cells reveals potential entities as targets for novel therapy.Scientific reports · 2024Article
- Identification of a potent PCNA-p15-interaction inhibitor by autodisplay-based peptide library screening.Microbial biotechnology · 2024Article
- Identification of a five genes prognosis signature for triple-negative breast cancer using multi-omics methods and bioinformatics analysis.Cancer gene therapy · 2022Article
- ELIMINATOR: essentiality analysis using multisystem networks and integer programming.BMC bioinformatics · 2022Article
- Modulation of POPDC1 Expression by Phenothiazine and Trifluoperazine Suppress Colon Cancer Growth and Migration.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Targeted EV to Deliver Chemotherapy to Treat Triple-Negative Breast Cancers.Pharmaceutics · 2022Article
- Role of CD47-SIRPα Checkpoint in Nanomedicine-Based Anti-Cancer Treatment.Frontiers in bioengineering and biotechnology · 2022Review
- Downregulation of the FBXO43 gene inhibits tumor growth in human breast cancer by limiting its interaction with PCNA.Journal of translational medicine · 2021Article
- Quantitative immunohistochemistry (IHC) analysis of biomarker combinations for human esophageal squamous cell carcinoma.Annals of translational medicine · 2021Article
- Targeting Non-Oncogene Addiction for Cancer Therapy.Biomolecules · 2021Review
- Post-Translational Modifications of PCNA in Control of DNA Synthesis and DNA Damage Tolerance-the Implications in Carcinogenesis.International journal of biological sciences · 2021Review
- Anti-EGFR antibody-drug conjugate for triple-negative breast cancer therapy.Engineering in life sciences · 2021Article
- Anti-cancer therapeutic benefit of red guava extracts as a potential therapy in combination with doxorubicin or targeted therapy for triple-negative breast cancer cells.International journal of medical sciences · 2020Article
- S100A1 blocks the interaction between p53 and mdm2 and decreases cell proliferation activity.PloS one · 2020Article
- Review
- The Anticancer Activity of a First-in-class Small-molecule Targeting PCNA.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- NKp44-Derived Peptide Binds Proliferating Cell Nuclear Antigen and Mediates Tumor Cell Death.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Tyrosine 211 (Y211) phosphorylation of proliferation cell nuclear antigen (PCNA) coincides with pronounced cancer cell proliferation and correlates with poor survival of breast cancer patients. In epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI)-resistant cells, both nuclear EGFR (nEGFR) expression and PCNA Y211 phosphorylation are increased. Moreover, the resistance to EGFR TKI is a major clinical problem in treating EGFR-overexpressing triple-negative breast cancer (TNBC). Thus, effective treatment to combat resistance is urgently needed. Here, we show that treatment of cell-penetrating PCNA peptide (CPPP) inhibits growth and induces apoptosis of human TNBC cells. The Y211F CPPP specifically targets EGFR and competes directly for PCNA tyrosine Y211 phosphorylation and prevents nEGFR from binding PCNA in vivo; it also suppresses tumor growth by sensitizing EGFR TKI resistant cells, which have enhanced nEGFR function and abrogated classical EGFR membrane signaling. Furthermore, we identify an active motif of CPPP, RFLNFF (RF6 CPPP), which is necessary and sufficient to inhibit TKI-resistant TNBC cell growth of orthotopic implanted tumor in mice. Finally, the activity of its synthetic retro-inverted derivative, D-RF6 CPPP, on an equimolar basis, is more potent than RF6 CPPP. Our study reveals a drug candidate with translational potential for the future development of safe and effective therapeutic for EGFR TKI resistance in TNBC.
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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.