ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2013
EZH2 promotes E2F-driven SCLC tumorigenesis through modulation of apoptosis and cell-cycle regulation.
Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 85 citations in OpenAlex.
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- Exploring the therapeutic potential of targeting polycomb repressive complex 2 in lung cancer.Frontiers in oncology · 2023Review
- Analysis of two-gene signatures and related drugs in small-cell lung cancer by bioinformatics.Open medicine (Warsaw, Poland) · 2023Article
- FBP1 knockdown decreases ovarian cancer formation and cisplatin resistance through EZH2-mediated H3K27me3.Bioscience reports · 2022Article
- Integrative Analysis for Identification of Therapeutic Targets and Prognostic Signatures in Non-Small Cell Lung Cancer.Bioinformatics and biology insights · 2022Article
- Signatures of plasticity, metastasis, and immunosuppression in an atlas of human small cell lung cancer.Cancer cell · 2021Article
- Identification of Potential Prognostic and Predictive Biomarkers for Immune-Checkpoint Inhibitor Response in Small Cell Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Evidence to Date: Evaluating Pembrolizumab in the Treatment of Extensive-Stage Small-Cell Lung Cancer.Clinics and practice · 2021Review
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
introductionAlthough enhancer of zeste homolog 2 (EZH2) has been associated with both non-small cell and small-cell lung cancers (SCLCs), current observations suggest different mechanisms of EZH2 activation and overexpression in these lung cancer types. Globally, SCLC kills 200,000 people yearly. New clinical approaches for SCLC treatment are required to improve the poor survival rate. Given the therapeutic potential of EZH2 as a target, we sought to delineate the downstream consequences of EZH2 disruption to identify the cellular mechanisms by which EZH2 promotes tumorigenesis in SCLC.
methodsWe generated cells with stable expression of short hairpin RNA targeting EZH2 and corresponding controls (pLKO.1) and determined the consequences of EZH2 knockdown on the cell cycle and apoptosis by means of propidium iodide staining and fluorescence-activated cell sorting, Western blot, quantitative reverse transcriptase-polymerase chain reaction as well as cell viability assessment using methylthiazol tetrazolium assays.
resultsWe discovered that EZH2 inhibition (1) increased apoptotic activity by up-regulating the proapoptotic factors Puma and Bad, (2) decreased the fraction of cells in S or G2/M phases, and (3) elevated p21 protein levels, implicating EZH2 in cell death and cell-cycle control in SCLC.
conclusionOur findings present evidence for the role of EZH2 in the regulation of cell cycle and apoptosis, providing a biological mechanism to explain the tumorigenicity of EZH2 in SCLC. Our work points to the great potential of EZH2 as a therapeutic target in SCLC.
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