Activating transcription factor 3 induces oxidative stress and genotoxicity, transcriptionally modulating metastasis-related gene expression in human papillomavirus-infected cervical cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Activating Transcription Factor 3 (ATF3) induces oxidative stress and DNA damage in cervical cancer cells, suppressing tumors. ATF3 also reduces metastasis by decreasing MMP1 expression, highlighting its therapeutic potential.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Activating Transcription Factor 3 (ATF3) exhibits tumor-suppressive functions in cervical cancer.
- ATF3's role in stress response and interaction with human papillomavirus (HPV) oncogenes is established.
- This study examines ATF3's effect on metastasis, oxidative stress, and DNA damage in HPV-positive cervical cancer.
Purpose Of The Study
- To investigate the regulatory impact of ATF3 on metastasis-related genes.
- To assess ATF3's influence on oxidative stress and DNA damage in cervical cancer cells.
- To explore ATF3's therapeutic potential in HPV-positive cervical cancer.
Main Methods
- Overexpression of ATF3 in HeLa and Ca Ski cell lines.
- Confirmation of ATF3 overexpression using Western blotting and RT-qPCR.
- Assessment of oxidative stress (ROS assays), DNA damage (Comet assays), and gene expression (RT-qPCR for HPV E6/E7, SHARP1, MMP1).
Main Results
- ATF3 overexpression elevated ROS levels, causing oxidative DNA damage and demonstrating cytotoxic effects.
- ATF3 significantly decreased MMP1 expression, suggesting an anti-metastatic role.
- SHARP1 and HPV E6/E7 expression remained unaffected, indicating selective gene modulation.
Conclusions
- ATF3 suppresses tumors in cervical cancer by inducing oxidative stress and DNA damage.
- ATF3 selectively targets metastasis-related genes, supporting its anti-metastatic potential.
- ATF3 is a promising therapeutic target for HPV-positive cervical cancer.
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