ArticleThe pharmacogenomics journal2010
Gene network analysis of oxidative stress-mediated drug sensitivity in resistant ovarian carcinoma cells.
Article in The pharmacogenomics journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Cloned Pig Fetuses Have a High Placental Lysophosphatidylcholine Level That Inhibits Trophoblast Cell Activity.Journal of developmental biology · 2025Article
- TRAP1 induced cisplatin resistance in gastric cancer cells by regulating oxidative stress.Frontiers in molecular biosciences · 2025Article
- Deciphering resistance mechanisms and novel strategies to overcome drug resistance in ovarian cancer: a comprehensive review.Oncology research · 2024Review
- Clinical implication and potential function of ARHGEF6 in acute myeloid leukemia: An in vitro study.PloS one · 2023Article
- Molecular and cellular paradigms of multidrug resistance in cancer.Cancer reports (Hoboken, N.J.) · 2022Review
- Targeting Redox Regulation as a Therapeutic Opportunity against Acute Leukemia: Pro-Oxidant Strategy or Antioxidant Approach?Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance.International journal of molecular sciences · 2021Review
- Targeting Nrf2 may reverse the drug resistance in ovarian cancer.Cancer cell international · 2021Review
- Insights into the Role of Oxidative Stress in Ovarian Cancer.Oxidative medicine and cellular longevity · 2021Review
- The significant role of redox system in myeloid leukemia: from pathogenesis to therapeutic applications.Biomarker research · 2020Review
- Overweight Women with Breast Cancer on Chemotherapy Have More Unfavorable Inflammatory and Oxidative Stress Profiles.Nutrients · 2020Article
- Antitumor Activity of New Olivacine Derivatives.Molecules (Basel, Switzerland) · 2020Article
- Prooxidative Activity of Celastrol Induces Apoptosis, DNA Damage, and Cell Cycle Arrest in Drug-Resistant Human Colon Cancer Cells.Oxidative medicine and cellular longevity · 2019Article
- The role of cellular reactive oxygen species in cancer chemotherapy.Journal of experimental & clinical cancer research : CR · 2018Review
- Article
- Evaluation of the cytotoxicity of the Bithionol - cisplatin combination in a panel of human ovarian cancer cell lines.BMC cancer · 2017Article
- New Challenges to Study Heterogeneity in Cancer Redox Metabolism.Frontiers in cell and developmental biology · 2017Review
- Article
- Defects in the Fanconi Anemia Pathway in Head and Neck Cancer Cells Stimulate Tumor Cell Invasion through DNA-PK and Rac1 Signaling.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Long-Term Alteration of Reactive Oxygen Species Led to Multidrug Resistance in MCF-7 Cells.Oxidative medicine and cellular longevity · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance in cancer cells involves complex molecular mechanisms and ovarian carcinoma cells become resistant to chlorambucil (Cbl) after continuous treatment. This drug- and ionizing radiation-resistant cells have lower level of endogenous ROS (reactive oxygen species) compared with sensitive cells. Elevation of the cellular ROS level by exogenous ROS generation increases the sensitivity of Cbl to resistant cells. In contrast, antioxidants prevent the sensitization of resistant cells to Cbl by H(2)O(2), COS (chronic oxidative stress) or NOO(-). The molecular mechanism of drug sensitivity with COS has been investigated by microarray gene expressions followed by gene network analysis and it reveals that a cdc42/rac1 guanine exchange factor, ARHGEF6, with p53 and DNA-Pkc (PRKDC) is central to induce apoptosis in Cbl(cos) (Cbl with COS) cells. mRNA and protein levels of major gene network pathway differ significantly in Cbl(cos) cells than in Cbl-treated cells. Moreover, DNA-PKc physically interacts with ARHGEF6 and p53 mostly in the nucleus of Cbl-treated cells, whereas in Cbl(cos)-treated cells, its interactions are mostly in the cytoplasm. These results suggest that low doses of Cbl and very low doses of COS together kill Cbl-resistant ovarian carcinoma cells and ARHGEF6 signaling may have an instrumental role in induction of apoptosis in Cbl(cos) cells.
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