ArticleThe Journal of biological chemistry2010
Activating transcription factor 3 activates p53 by preventing E6-associated protein from binding to E6.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptional factor ATF3 impairs KSHV lytic replication by suppressing the expression of viral bZIP protein K8.PLoS pathogens · 2026Article
- Cervical Cancer in the Era of HPV: Translating Molecular Mechanisms into Preventive Public Health Action.International journal of molecular sciences · 2025Review
- Inhibition of p16 and NF-κB Oncogenic Activity in Human Papillomavirus-Infected Cervical Cancer Cells: A New Role for Activating Transcription Factor-3.The Yale journal of biology and medicine · 2025Article
- Activating transcription factor 3 mediates apoptosis and cell cycle arrest in TP53-mutated anaplastic thyroid cancer cells.Thyroid research · 2024Article
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- Activating transcription factor 3 inhibits NF‑κB p65 signaling pathway and mediates apoptosis and cell cycle arrest in cervical cancer cells.Infectious agents and cancer · 2022Article
- Activating transcription factor 3 mediates apoptotic functions through a p53-independent pathway in human papillomavirus 18 infected HeLa cells.Virus genes · 2022Article
- Induction of heparanase 2 (Hpa2) expression by stress is mediated by ATF3.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Genome-Wide Identification, Comparison, and Expression Analysis of Transcription Factors in AscidianInternational journal of molecular sciences · 2021Article
- ATF3 deficiency impairs the proliferative-secretory phase transition and decidualization in RIF patients.Cell death & disease · 2021Article
- Protective Effect of Pyxinol, One Active Ingredient ofFrontiers in pharmacology · 2021Article
- Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection.PLoS pathogens · 2020Article
- The mechanism of ATF3 repression of epithelial-mesenchymal transition and suppression of cell viability in cholangiocarcinoma via p53 signal pathway.Journal of cellular and molecular medicine · 2019Article
- Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells.PloS one · 2019Article
- Physiological/pathological ramifications of transcription factors in the unfolded protein response.Genes & development · 2017Review
- Activating transcription factor 3 is crucial for antitumor activity and to strengthen the antiviral properties of Onconase.Oncotarget · 2017Article
- Echinacoside Protects Against MPP(+)-Induced Neuronal Apoptosis via ROS/ATF3/CHOP Pathway Regulation.Neuroscience bulletin · 2016Article
- HPV16 E6 upregulates Aurora A expression.Oncology letters · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Genomic integration of human papillomavirus (HPV) DNA accounts for more than 90% of cervical cancers. High-risk genital HPVs encode E6 proteins that can interact with a cellular ubiquitin ligase E6-associated protein (E6AP) and target the tumor suppressor p53 for ubiquitin-mediated proteolysis. Currently, how this critical event is regulated is largely unknown. Here we report that activating transcription factor 3 (ATF3), a broad DNA damage sensor whose expression is frequently downregulated in cervical cancer, interacted with E6 and prevented p53 from ubiquitination and degradation mediated by the viral protein. Consistent with its role as a potent E6 antagonist, ATF3 expressed enforcedly in HPV-positive SiHa cells activated p53, leading to expression of p53-target genes (e.g. p21 and PUMA), cell cycle arrest and apoptotic cell death. The leucine zipper domain of ATF3 appears indispensable for these effects as an ATF3 mutant lacking this domain failed to interact with E6 and activate p53 in the cervical cancer cells. The prevention of p53 degradation was unlikely caused by binding of ATF3 to the tumor suppressor, but rather was a consequence of disruption of the E6-E6AP interaction by ATF3. These results indicate that ATF3 plays a key role in a mechanism defending against HPV-induced carcinogenesis, and could serve as a novel therapeutic target for HPV-positive cancers.
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