ArticleCancer discovery2015
Suppression of CHK1 by ETS Family Members Promotes DNA Damage Response Bypass and Tumorigenesis.
Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Novel frontiers in urogenital cancers: from molecular bases to preclinical models to tailor personalized treatments in ovarian and prostate cancer patients.Journal of experimental & clinical cancer research : CR · 2024Review
- Bibliometric analysis of PTEN in neurodevelopment and neurodegeneration.Frontiers in aging neuroscience · 2024Article
- Article
- In Vivo Models for Prostate Cancer Research.Cancers · 2022Review
- HGF-mediated elevation of ETV1 facilitates hepatocellular carcinoma metastasis through upregulating PTK2 and c-MET.Journal of experimental & clinical cancer research : CR · 2022Article
- Identification of hub genes and their correlation with infiltration of immune cells inFrontiers in immunology · 2022Article
- Patient-matched analysis identifies deregulated networks in prostate cancer to guide personalized therapeutic intervention.American journal of cancer research · 2021Article
- Calcium cytotoxicity sensitizes prostate cancer cells to standard-of-care treatments for locally advanced tumors.Cell death & disease · 2020Article
- Function and regulation of the PEA3 subfamily of ETS transcription factors in cancer.American journal of cancer research · 2020Review
- Comparative RNA-seq analysis reveals dys-regulation of major canonical pathways in ERG-inducible LNCaP cell progression model of prostate cancer.Oncotarget · 2019Article
- Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors.Oncotarget · 2019Review
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2.Immunity · 2018Article
- Prostate-derived ETS factor improves prognosis and represses proliferation and invasion in hepatocellular carcinoma.Oncotarget · 2017Article
- Roles and regulations of the ETS transcription factor ELF4/MEF.Journal of molecular cell biology · 2017Review
- Chk1 Promotes DNA Damage Response Bypass following Oxidative Stress in a Model of Hydrogen Peroxide-Associated Ulcerative Colitis through JNK Inactivation and Chromatin Binding.Oxidative medicine and cellular longevity · 2017Article
- Distinct outcomes of CRL-Nedd8 pathway inhibition reveal cancer cell plasticity.Cell death & disease · 2016Article
- Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines.Pigment cell & melanoma research · 2016Article
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledThe ETS family of transcription factors has been repeatedly implicated in tumorigenesis. In prostate cancer, ETS family members, such as ERG, ETV1, ETV4, and ETV5, are frequently overexpressed due to chromosomal translocations, but the molecular mechanisms by which they promote prostate tumorigenesis remain largely undefined. Here, we show that ETS family members, such as ERG and ETV1, directly repress the expression of the checkpoint kinase 1 (CHK1), a key DNA damage response cell-cycle regulator essential for the maintenance of genome integrity. Critically, we find that ERG expression correlates with CHK1 downregulation in human patients and demonstrate that Chk1 heterozygosity promotes the progression of high-grade prostatic intraepithelial neoplasia into prostatic invasive carcinoma in Pten(+) (/-) mice. Importantly, CHK1 downregulation sensitizes prostate tumor cells to etoposide but not to docetaxel treatment. Thus, we identify CHK1 as a key functional target of the ETS proto-oncogenic family with important therapeutic implications. SIGNIFICANCE: Genetic translocation and aberrant expression of ETS family members is a common event in different types of human tumors. Here, we show that through the transcriptional repression of CHK1, ETS factors may favor DNA damage accumulation and consequent genetic instability in proliferating cells. Importantly, our findings provide a rationale for testing DNA replication inhibitor agents in ETS-positive TP53-proficient tumors.
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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.