ArticleBioMed research international2014
Cellular levels of oxidative stress affect the response of cervical cancer cells to chemotherapeutic agents.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 62 citations in OpenAlex.
- Mesenchymal Stem Cell-Derived Exosomes Reprogram Chemosensitivity Pathways in Cervical Cancer Spheroids.International journal of molecular sciences · 2026Article
- Redox-active nitroxides enhance cisplatin efficacy against cervical cancer.Redox biology · 2026Article
- An innovative glutamine metabolism-related gene signature for predicting prognosis and immune landscape in cervical cancer.Discover oncology · 2025Article
- Synergistic celecoxib and dimethyl-celecoxib combinations block cervix cancer growth through multiple mechanisms.PloS one · 2024Article
- Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2023Review
- ComparativeACS omega · 2023Article
- Review
- Gene Promoter-Methylation Signature as Biomarker to Predict Cisplatin-Radiotherapy Sensitivity in Locally Advanced Cervical Cancer.Frontiers in oncology · 2022Article
- Role of NRF2 cascade in determining the differential response of cervical cancer cells to anticancer drugs: an in vitro study.Molecular biology reports · 2022Article
- Albendazole Release from Silica-Chitosan Nanospheres. In Vitro Study on Cervix Cancer Cell Lines.Polymers · 2021Article
- Hypoxia, oxidative stress, and immune evasion: a trinity of the trichothecenes T-2 toxin and deoxynivalenol (DON).Archives of toxicology · 2021Review
- PARP1-Inhibition Sensitizes Cervical Cancer Cell Lines for Chemoradiation and Thermoradiation.Cancers · 2021Article
- ROS-dependent HIF1α activation under forced lipid catabolism entails glycolysis and mitophagy as mediators of higher proliferation rate in cervical cancer cells.Journal of experimental & clinical cancer research : CR · 2021Article
- Inhibition of kinase IKKβ suppresses cellular abnormalities induced by the human papillomavirus oncoprotein HPV 18E6.Scientific reports · 2021Article
- Inhibition of Inducible Nitric Oxide Synthase (iNOS) by Andrographolide andOxidative medicine and cellular longevity · 2021Article
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- A reactive oxygen species scoring system predicts cisplatin sensitivity and prognosis in ovarian cancer patients.BMC cancer · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment of advanced and relapsed cervical cancer is frequently ineffective, due in large part to chemoresistance. To examine the pathways responsible, we employed the cervical carcinoma-derived SiHa and CaSki cells as cellular models of resistance and sensitivity, respectively, to treatment with chemotherapeutic agents, doxorubicin, and cisplatin. We compared the proteomic profiles of SiHa and CaSki cells and identified pathways with the potential to contribute to the differential response. We then extended these findings by comparing the expression level of genes involved in reactive oxygen species (ROS) metabolism through the use of a RT-PCR array. The analyses demonstrated that the resistant SiHa cells expressed higher levels of antioxidant enzymes. Decreasing or increasing oxidative stress led to protection or sensitization, respectively, in both cell lines, supporting the idea that cellular levels of oxidative stress affect responsiveness to treatment. Interestingly, doxorubicin and cisplatin induced different profiles of ROS, and these differences appear to contribute to the sensitivity to treatment displayed by cervical cancer cells. Overall, our findings demonstrate that cervical cancer cells display variable profiles with respect to their redox-generating and -adaptive systems, and that these different profiles have the potential to contribute to their responses to treatments with chemotherapy.
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