ArticleExperimental & molecular medicine2015
An important role for peroxiredoxin II in survival of A549 lung cancer cells resistant to gefitinib.
Article in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
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- Promoting reactive oxygen species accumulation to overcome tyrosine kinase inhibitor resistance in cancer.Cancer cell international · 2024Review
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- BRM270 targets cancer stem cells and augments chemo-sensitivity in cancer.Oncology letters · 2020Review
- Bidirectional interaction of lncRNA AFAP1-AS1 and CRKL accelerates the proliferative and metastatic abilities of hepatocarcinoma cells.Journal of advanced research · 2020Article
- The Double-Faced Role of Nitric Oxide and Reactive Oxygen Species in Solid Tumors.Antioxidants (Basel, Switzerland) · 2020Review
- A Novel Benzofuran Derivative Moracin N Induces Autophagy and Apoptosis Through ROS Generation in Lung Cancer.Frontiers in pharmacology · 2020Article
- Peroxiredoxins and Immune Infiltrations in Colon Adenocarcinoma: Their Negative Correlations and Clinical Significances, an In Silico Analysis.Journal of Cancer · 2020Article
- miR-762 activation confers acquired resistance to gefitinib in non-small cell lung cancer.BMC cancer · 2019Article
- Peroxiredoxins and Beyond; Redox Systems Regulating Lung Physiology and Disease.Antioxidants & redox signaling · 2019Review
- Peroxiredoxin II Regulates Cancer Stem Cells and Stemness-Associated Properties of Cancers.Cancers · 2018Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- BRM270 inhibits cancer stem cell maintenance via microRNA regulation in chemoresistant A549 lung adenocarcinoma cells.Cell death & disease · 2018Article
- Proteomic analysis of serum deprivation in tongue squamous cell carcinoma.Molecular medicine reports · 2017Article
- The role of peroxiredoxins in cancer.Molecular and clinical oncology · 2017Article
- Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy.Oxidative medicine and cellular longevity · 2017Review
- Epigenetic regulation of peroxiredoxins: Implications in the pathogenesis of cancer.Experimental biology and medicine (Maywood, N.J.) · 2017Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Redox adaptation is an important concept that explains the mechanisms by which cancer cells survive under persistent endogenous oxidative stress and become resistant to certain anticancer agents. To investigate this concept, we determined the expression levels of peroxiredoxins (Prxs), antioxidant enzymes in drug-resistant non-small cell lung carcinoma cells. Prx II was remarkably increased only in A549/GR (gefitinib-resistant) cells compared with A549 cells, consistent with methylation/demethylation. Prx II was highly methylated in the A549 cells but was demethylated in the A549/GR cells. The elevated expression of Prx II resulted in the downregulation of reactive oxygen species (ROS) and cell death and upregulation of cell cycle progression in the A549/GR cells. When Prx II mRNA in the A549/GR cells was knocked down, the levels of ROS and apoptosis were significantly recovered to the levels of the controls. In addition, signaling molecules involved in apoptosis were increased in the A549/GR-shPrx II cells. There was no difference in the expression of MAPK/ERK between the A549/GR cells and A549/GR-shPrx II cells, but the phosphorylation of JNK was increased in the A549/GR cells and was markedly decreased in the A549/GR-shPrx II cells. Colony number and tumor growth were significantly decreased in the A549/GR-shPrx II cells compared with the A549/GR cells. Our findings suggest that Prx II has an important role in cancer cell survival via the modulation of signaling molecules involved in apoptosis and the phosphorylation of JNK by the downregulation of ROS levels in A549/GR cells.
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