ArticleThe American journal of pathology2009
Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- SRF Rearrangements in Soft Tissue Tumors with Muscle Differentiation.Biomolecules · 2022Article
- E2F1: Cause and Consequence of DNA Replication Stress.Frontiers in molecular biosciences · 2020Review
- Implications of Oxidative Stress and Cellular Senescence in Age-Related Thymus Involution.Oxidative medicine and cellular longevity · 2020Review
- Melatonin: an anti-tumor agent for osteosarcoma.Cancer cell international · 2019Review
- Integrating the DNA damage and protein stress responses during cancer development and treatment.The Journal of pathology · 2018Review
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.BMC cancer · 2018Article
- Hypoxia driven glycation: Mechanisms and therapeutic opportunities.Seminars in cancer biology · 2018Review
- A prototypical non-malignant epithelial model to study genome dynamics and concurrently monitor micro-RNAs and proteins in situ during oncogene-induced senescence.BMC genomics · 2018Article
- E2F1 silencing inhibits migration and invasion of osteosarcoma cells via regulating DDR1 expression.International journal of oncology · 2017Article
- Robust, universal biomarker assay to detect senescent cells in biological specimens.Aging cell · 2017Article
- WWOX and p53 Dysregulation Synergize to Drive the Development of Osteosarcoma.Cancer research · 2016Article
- Chronic p53-independent p21 expression causes genomic instability by deregulating replication licensing.Nature cell biology · 2016Article
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- Hepatitis B Virus X Protein Upregulates hELG1/ ATAD5 Expression through E2F1 in Hepatocellular Carcinoma.International journal of biological sciences · 2016Article
- E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo.World journal of gastroenterology · 2015Article
- E2F transcription factors and digestive system malignancies: how much do we know?World journal of gastroenterology · 2014Article
- Steroid receptor co-activator-3 promotes osteosarcoma progression through up-regulation of FoxM1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- E2F1-mediated DNA damage is implicated in 8-Cl-adenosine-induced chromosome missegregation and apoptosis in human lung cancer H1299 cells.Molecular and cellular biochemistry · 2013Article
- Functional interplay between the DNA-damage-response kinase ATM and ARF tumour suppressor protein in human cancer.Nature cell biology · 2013Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 6 countries.
Funding
Abstract
Osteosarcoma is the most common primary bone cancer. Mutations of the RB gene represent the most frequent molecular defect in this malignancy. A major consequence of this alteration is that the activity of the key cell cycle regulator E2F1 is unleashed from the inhibitory effects of pRb. Studies in animal models and in human cancers have shown that deregulated E2F1 overexpression possesses either "oncogenic" or "oncosuppressor" properties, depending on the cellular context. To address this issue in osteosarcomas, we examined the status of E2F1 relative to cell proliferation and apoptosis in a clinical setting of human primary osteosarcomas and in E2F1-inducible osteosarcoma cell line models that are wild-type and deficient for p53. Collectively, our data demonstrated that high E2F1 levels exerted a growth-suppressing effect that relied on the integrity of the DNA damage response network. Surprisingly, induction of p73, an established E2F1 target, was also DNA damage response-dependent. Furthermore, a global proteome analysis associated with bioinformatics revealed novel E2F1-regulated genes and potential E2F1-driven signaling networks that could provide useful targets in challenging this aggressive neoplasm by innovative therapies.
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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.