ArticleCancer research2019
Disruption of the Rbm38-eIF4E Complex with a Synthetic Peptide Pep8 Increases p53 Expression.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 42 citations in OpenAlex.
- RBM protein family: Focusing on the occurrence, progression and treatment of cancer.Medical oncology (Northwood, London, England) · 2026Review
- Review
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Processes and therapeutic perspectives of acylation modifications of lysine and cysteine in tumors.Cell communication and signaling : CCS · 2026Review
- RNA-binding protein Rbm38 as a multifaceted post-transcriptional regulator in zebrafish pancreatic development.Journal of molecular cell biology · 2026Article
- Article
- Downregulation of ZFP36L1 contributes to methotrexate resistance in osteosarcoma through enhanced NHEJ DNA repair mechanisms.Cell death & disease · 2025Article
- ANGEL2 Modulates Wild-type TP53 Translation and Doxorubicin Chemosensitivity in Colon Cancer.Molecular cancer research : MCR · 2025Article
- TRIM21-driven K63-linked ubiquitination of RBM38c, as a novel interactor of BECN1, contributes to DNA damage-induced autophagy.Cell death and differentiation · 2025Article
- Article
- Rbm24-mediated post-transcriptional regulation of skeletal and cardiac muscle development, function and regeneration.Journal of muscle research and cell motility · 2025Review
- Role of artificial intelligence in cancer detection using protein p53: A Review.Molecular biology reports · 2024Review
- Dysregulated RBM24 phosphorylation impairs APOE translation underlying psychological stress-induced cardiovascular disease.Nature communications · 2024Article
- Article
- Understanding crosstalk of organ tropism, tumor microenvironment and noncoding RNAs in breast cancer metastasis.Molecular biology reports · 2023Review
- Surmounting Cancer Drug Resistance: New Perspective on RNA-Binding Proteins.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Identification of a First-in-Class Small-Molecule Inhibitor of the EIF4E-RBM38 Complex That Enhances Wild-type TP53 Protein Translation for Tumor Growth Suppression.Molecular cancer therapeutics · 2023Article
- The nexus between RNA-binding proteins and their effectors.Nature reviews. Genetics · 2023Review
- Novel roles of RNA-binding proteins in drug resistance of breast cancer: from molecular biology to targeting therapeutics.Cell death discovery · 2023Review
- RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.Advanced drug delivery reviews · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Rbm38 is a p53 target and an RNA-binding protein known to suppress p53 translation by preventing eukaryotic translation initiation factor 4E (eIF4E) from binding to p53 mRNA. In this study, we show that synthetic peptides corresponding to the binding interface between Rbm38 and eIF4E, including an 8 amino acid peptide (Pep8) derived from Rbm38, are effective in relieving Rbm38-mediated repression of p53. Molecular simulations showed that Ser-6 in Pep8 forms a hydrogen bond with Asp-202 in eIF4E. Substitution of Ser-6 with Lys, but not with Asp, enhanced the ability of Pep8 to inhibit the Rbm38-eIF4E complex. Importantly, Pep8 alone or together with a low dose of doxorubicin potently induced p53 expression and suppressed colony and tumor sphere formation and xenograft tumors in Rbm38- and p53-dependent manners. Together, we conclude that modulating the Rbm38-eIF4E complex may be explored as a therapeutic strategy for cancers that carry wild-type p53. SIGNIFICANCE: Disruption of the Rbm38-eIF4E complex via synthetic peptides induces wild-type p53 expression, suppresses tumor growth and progression, and may serve as a novel cancer therapeutic strategy.
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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.