ArticleVirology journal2025
Activating transcription factor 3 induces oxidative stress and genotoxicity, transcriptionally modulating metastasis-related gene expression in human papillomavirus-infected cervical cancer.
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recurrent PIK3CA-E545K mutation promotes cervical cancer growth and invasion via AKT/mTOR signaling.Molecular genetics and genomics : MGG · 2026Article
- Integrated genomic and proteomic profiling reveals insights into chemoradiation resistance in cervical cancer.Molecular oncology · 2026Article
- Cervical human papillomavirus: the therapeutic target of botanical drugs.Frontiers in pharmacology · 2026Review
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4 authors.
Funding
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Abstract
backgroundActivating Transcription Factor 3 (ATF3) is known for its tumor-suppressive properties in cervical cancer, particularly through its role in stress response and interactions with human papillomavirus (HPV) oncogenes. This study investigates ATF3's regulatory impact on metastasis-related genes, oxidative stress, and DNA damage in HPV-positive cervical cancer cells.
methodsHeLa and Ca Ski cell lines were transfected with ATF3-expressing vectors. Western blotting and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were used to confirm ATF3 overexpression following transfection. ROS assays and Comet assays assessed the impact of ATF3 on oxidative stress and DNA damage, while RT-qPCR was used to evaluate changes in HPV E6/E7, SHARP1, and MMP1 gene expression.
resultsATF3 overexpression led to elevated ROS levels (p < 0.02), resulting in oxidative DNA damage. These results demonstrate ATF3's cytotoxic impact on cervical cancer cells through oxidative stress and DNA damage. Additionally, ATF3 overexpression significantly decreased MMP1 expression (p < 0.03), indicating a potential anti-metastatic effect, while SHARP1 and HPV E6/E7 expression levels were not significantly altered, indicating selective gene modulation by ATF3.
conclusionThese findings reveal that ATF3 contributes to tumor suppression in cervical cancer by modulating oxidative stress and DNA damage, selectively targeting genes involved in metastasis. These findings supports ATF3's role in regulating key pathways in HPV-positive cervical cancer cells, providing a basis for further exploration of ATF3 as a target in therapeutic strategies aimed at improving outcomes in cervical cancer.
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