ArticleNature communications2023
YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells.
Article in Nature communications, 2023. 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, 37 citations in OpenAlex.
- Article
- YBX1 Confers immunosuppressive bone metastatic traits in non-small cell lung cancer.Nature communications · 2026Article
- EIF4A3/circPTGR1/miR-4725-5p positive- feedback loop promotes colorectal cancer progression via FAK/AKT signaling pathway.Molecular cancer · 2026Article
- YBX1 as an adaptive RNA hub in cancer: linking state-dependent RNA regulation to tumor immunity, metabolic reprogramming, and therapy resistance.Frontiers in immunology · 2026Review
- BFAR Promotes Neutrophil Infiltration and Immunosuppressive Reprogramming through the PRP19-YBX1 Axis to Induce Immune Evasion in Gastric Cancer.Cancer immunology research · 2025Article
- SwitchTFI: identifying transcription factors driving cell differentiation.Genome biology · 2025Article
- A patient-derived orthotopic xenograft model unveils metastatic dynamics in head and neck squamous cell carcinoma.The FEBS journal · 2025Article
- Targeting the Phosphoinositide 3-Kinase/Protein Kinase B Pathway Suppresses Y-Box Binding Protein 1 Expression and Inhibits Colorectal Cancer Progression.World journal of oncology · 2025Article
- Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis.Cancer gene therapy · 2025Article
- EPS8L2 drives colorectal cancer cell proliferation and migration via YBX1-dependent activation of G3BP2 transcription.Cell death & disease · 2025Article
- The Therapeutic Potential of Bombyx Batryticatus for Chronic Atrophic Gastritis Precancerous Lesions via the PI3K/AKT/mTOR Pathway Based on Network Pharmacology of Blood-Entering Components.Pharmaceuticals (Basel, Switzerland) · 2025Article
- KAT7-acetylated YBX1 promotes hepatocellular carcinoma proliferation by reprogramming nucleotide metabolism.BMC cancer · 2025Article
- Autophagy Deficiency Induced by SAT1 Potentiates Tumor Progression in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Navigating therapeutic strategies: HPV classification in head and neck cancer.British journal of cancer · 2024Review
- Integrated single-cell and spatial transcriptomic analysis reveals YBX1 drives immune regulation in GBM progression.Heliyon · 2024Article
- Y-Box Binding Protein 1: Unraveling the Multifaceted Role in Cancer Development and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Design, synthesis, and biological evaluation of 2,4-dimorpholinopyrimidine-5-carbonitrile derivatives as orally bioavailable PI3K inhibitors.Frontiers in pharmacology · 2024Article
- Comprehensive pan-cancer analysis of YBX family reveals YBX2 as a potential biomarker in liver cancer.Frontiers in immunology · 2024Article
- RP11-296E3.2 acts as an important molecular chaperone for YBX1 and promotes colorectal cancer proliferation and metastasis by activating STAT3.Journal of translational medicine · 2023Article
- Recent advances in tumor targeted polymeric nanoparticles for HNC treatment: Enhancing therapeutic efficacy via engineered and biocompatible drug delivery systems.Journal of oral biology and craniofacial researchReview
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In heterogeneous head and neck cancer (HNC), subtype-specific treatment regimens are currently missing. An integrated analysis of patient HNC subtypes using single-cell sequencing and proteome profiles reveals an epithelial-mesenchymal transition (EMT) signature within the epithelial cancer-cell population. The EMT signature coincides with PI3K/mTOR inactivation in the mesenchymal subtype. Conversely, the signature is suppressed in epithelial cells of the basal subtype which exhibits hyperactive PI3K/mTOR signalling. We further identify YBX1 phosphorylation, downstream of the PI3K/mTOR pathway, restraining basal-like cancer cell proliferation. In contrast, YBX1 acts as a safeguard against the proliferation-to-invasion switch in mesenchymal-like epithelial cancer cells, and its loss accentuates partial-EMT and in vivo invasion. Interestingly, phospho-YBX1 that is mutually exclusive to partial-EMT, emerges as a prognostic marker for overall patient outcomes. These findings create a unique opportunity to sensitise mesenchymal cancer cells to PI3K/mTOR inhibitors by shifting them towards a basal-like subtype as a promising therapeutic approach against HNC.
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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.