ArticleVirus genes2022
Activating transcription factor 3 mediates apoptotic functions through a p53-independent pathway in human papillomavirus 18 infected HeLa cells.
Article in Virus genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Genotype-driven variations in lncRNA expression underlie predisposition to high-grade serous ovarian cancer.Journal of advanced research · 2026Article
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- 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 induces oxidative stress and genotoxicity, transcriptionally modulating metastasis-related gene expression in human papillomavirus-infected cervical cancer.Virology journal · 2025Article
- Activation of ATF3 via the integrated stress response pathway regulates innate immune response to restrict Zika virus.Journal of virology · 2024Article
- Activating transcription factor 3 mediates apoptosis and cell cycle arrest in TP53-mutated anaplastic thyroid cancer cells.Thyroid research · 2024Article
- Activation of ATF3 via the Integrated Stress Response Pathway Regulates Innate Immune Response to Restrict Zika Virus.bioRxiv : the preprint server for biology · 2024Article
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- Design, Synthesis, andAnti-cancer agents in medicinal chemistry · 2024Article
- 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
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activating transcription factor 3 (ATF3) is the first p53 stability regulator that interferes with the ubiquitination of p53. However, the E6 oncoprotein of high-risk human papillomaviruses (HPVs) binds to and induces proteasome-dependent degradation of the host p53 protein. Herein, we investigate the effects of ATF3 overexpression on cell cycle progression and apoptosis in HPV-18-infected HeLa cells, and further examine whether ATF3 could alter the apoptosis level of HeLa cells through the inhibition of E6-mediated p53 degradation. Cytological function of HeLa cells prior and subsequent to the overexpression of ATF3 was assessed using cell cycle and annexin V/PI flow cytometry analysis. Western blotting assays revealed no significant effect of ATF3 on the levels of p53 and E6 in HeLa cells. However, annexin V staining demonstrated increases in apoptosis. ATF3 acts as a tumor suppressor factor in HPV18-related cervical cancer which mediates apoptotic functions through a p53-independent pathway.
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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.