ArticleOncogene2017
EZH2-mediated upregulation of ROS1 oncogene promotes oral cancer metastasis.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Clustering and a conformational switch drive activation of the mammalian receptor tyrosine kinase ROS1.Nature communications · 2026Article
- Dynamic Evolution of the Tumor Immune Microenvironment in Malignant Tumors and Emerging Therapeutic Paradigms.MedComm · 2025Review
- Normal bronchial field basal cells show persistent methylome-wide impact of tobacco smoking, including in known cancer genes.Epigenetics · 2025Article
- Squamocin Suppresses Tumor Growth through Triggering an Endoplasmic Reticulum Stress-Associated Degradation of EZH2/MYC Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular Mechanisms of ARD1 in Tumors.Cancer medicine · 2025Review
- Proteogenomic characterisation of primary oral cancer unveils extracellular matrix remodelling and immunosuppressive microenvironment linked to lymph node metastasis.Clinical and translational medicine · 2025Article
- The power and the promise of epigenetic drugs in oncology.Frontiers in genetics · 2025Review
- Molecular insight into histone methylation as a novel target for oral squamous cell carcinoma: future hope in personalised medicine.Journal of Cancer · 2025Review
- Analysis of CD74 Occurrence in Oncogenic Fusion Proteins.International journal of molecular sciences · 2023Review
- New insights into RAS in head and neck cancer.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- NOTCH pathway inactivation reprograms stem-like oral cancer cells to JAK-STAT dependent state and provides the opportunity of synthetic lethality.Translational oncology · 2023Article
- Role of epigenetics in OSCC: an understanding above genetics.Medical oncology (Northwood, London, England) · 2023Review
- PRC2 loss drives MPNST metastasis and matrix remodeling.JCI insight · 2022Article
- N-α-Acetyltransferase 10 inhibits invasion and metastasis of oral squamous cell carcinoma via regulating Pirh2-p53 signalling pathway.Journal of cellular and molecular medicine · 2022Article
- Comprehensive Molecular Landscape of Cetuximab Resistance in Head and Neck Cancer Cell Lines.Cells · 2022Article
- LINC00662 Promotes Oral Squamous Cell Carcinoma Cell Growth and Metastasis through miR-144-3p/EZH2 Axis.Yonsei medical journal · 2021Article
- Targeting epigenetic modulation of cholesterol synthesis as a therapeutic strategy for head and neck squamous cell carcinoma.Cell death & disease · 2021Article
- ROS1-dependent cancers - biology, diagnostics and therapeutics.Nature reviews. Clinical oncology · 2021Review
- Mitochondrial ROS1 Increases Mitochondrial Fission and Respiration in Oral Squamous Cancer Carcinoma.Cancers · 2020Article
- Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current anti-epidermal growth factor receptor (EGFR) therapy for oral cancer does not provide satisfactory efficacy due to drug resistance or reduced EGFR level. As an alternative candidate target for therapy, here we identified an oncogene, ROS1, as an important driver for oral squamous cell carcinoma (OSCC) metastasis. Among tumors from 188 oral cancer patients, upregulated ROS1 expression strongly correlated with metastasis to lung and lymph nodes. Mechanistic studies uncover that the activated ROS1 results from highly expressed ROS1 gene instead of gene rearrangement, a phenomenon distinct from other cancers. Our data further reveal a novel mechanism that reduced histone methyltransferase EZH2 leads to a lower trimethylation of histone H3 lysine 27 suppressive modification, relaxes chromatin, and promotes the accessibility of the transcription factor STAT1 to the enhancer and the intron regions of ROS1 target genes, CXCL1 and GLI1, for upregulating their expressions. Down-regulation of ROS1 in highly invasive OSCC cells, nevertheless, reduces cell proliferation and inhibits metastasis to lung in the tail-vein injection and the oral cavity xenograft models. Our findings highlight ROS1 as a candidate biomarker and therapeutic target for OSCC. Finally, we demonstrate that co-targeting of ROS1 and EGFR could potentially offer an effective oral cancer therapy.
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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.