ArticlePloS one2010
Molecular decoy to the Y-box binding protein-1 suppresses the growth of breast and prostate cancer cells whilst sparing normal cell viability.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- YBX1 as a developmental regulator of ventricular morphogenesis and a potential target in cardiac pathology.American journal of physiology. Heart and circulatory physiology · 2026Article
- Integrative Investigation of Flavonoids Targeting YBX1 Protein-Protein Interaction Network in Breast Cancer: From Computational Analysis to Experimental Validation.Molecular biotechnology · 2025Article
- Therapeutic Potential of Decoys for Prostate Cancers: A Review of Recent Updates.Current medicinal chemistry · 2024Review
- YB-1 activating cascades as potential targets in KRAS-mutated tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Review
- Article
- RNA-binding proteins and their role in kidney disease.Nature reviews. Nephrology · 2022Review
- The role of the p90 ribosomal S6 kinase family in prostate cancer progression and therapy resistance.Oncogene · 2021Review
- Stress-induced tunneling nanotubes support treatment adaptation in prostate cancer.Scientific reports · 2019Article
- Oncogenic Y-box binding protein-1 as an effective therapeutic target in drug-resistant cancer.Cancer science · 2019Review
- Why Be One Protein When You Can Affect Many? The Multiple Roles of YB-1 in Lung Cancer and Mesothelioma.Frontiers in cell and developmental biology · 2019Review
- Fisetin targets YB-1/RSK axis independent of its effect on ERK signaling: insights from in vitro and in vivo melanoma models.Scientific reports · 2018Article
- Role of Y Box Protein-1 in cancer: As potential biomarker and novel therapeutic target.Journal of Cancer · 2017Review
- GOLPH3 and YB-1 Are Novel Markers Correlating With Poor Prognosis in Prostate Cancer.World journal of oncology · 2015Article
- Y-Box Binding Protein 1 Stabilizes Hepatitis C Virus NS5A via Phosphorylation-Mediated Interaction with NS5A To Regulate Viral Propagation.Journal of virology · 2015Article
- Prognostic role of YB-1 expression in breast cancer: a meta-analysis.International journal of clinical and experimental medicine · 2015Article
- YB-1 expression promotes epithelial-to-mesenchymal transition in prostate cancer that is inhibited by a small molecule fisetin.Oncotarget · 2014Article
- Targeted therapy for breast cancer prevention.Frontiers in oncology · 2013Review
- Trilayer micelles for combination delivery of rapamycin and siRNA targeting Y-box binding protein-1 (siYB-1).Biomaterials · 2013Article
- Article
- Impact of oncogenic K-RAS on YB-1 phosphorylation induced by ionizing radiation.Breast cancer research : BCR · 2011Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The Y-box binding protein-1 (YB-1) is an oncogenic transcription/translation factor that is activated by phosphorylation at S102 whereby it induces the expression of growth promoting genes such as EGFR and HER-2. We recently illustrated by an in vitro kinase assay that a novel peptide to YB-1 was highly phosphorylated by the serine/threonine p90 S6 kinases RSK-1 and RSK-2, and to a lesser degree PKCα and AKT. Herein, we sought to develop this decoy cell permeable peptide (CPP) as a cancer therapeutic. This 9-mer was designed as an interference peptide that would prevent endogenous YB-1(S102) phosphorylation based on molecular docking. In cancer cells, the CPP blocked P-YB-1(S102) and down-regulated both HER-2 and EGFR transcript level and protein expression. Further, the CPP prevented YB-1 from binding to the EGFR promoter in a gel shift assay. Notably, the growth of breast (SUM149, MDA-MB-453, AU565) and prostate (PC3, LNCap) cancer cells was inhibited by ∼90% with the CPP. Further, treatment with this peptide enhanced sensitivity and overcame resistance to trastuzumab in cells expressing amplified HER-2. By contrast, the CPP had no inhibitory effect on the growth of normal immortalized breast epithelial (184htert) cells, primary breast epithelial cells, nor did it inhibit differentiation of hematopoietic progenitors. These data collectively suggest that the CPP is a novel approach to suppressing the growth of cancer cells while sparing normal cells and thereby establishes a proof-of-concept that blocking YB-1 activation is a new course of cancer therapeutics.
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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.