ArticleMolecular cancer research : MCR2012
Acquisition of resistance of pancreatic cancer cells to 2-methoxyestradiol is associated with the upregulation of manganese superoxide dismutase.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Potential role of hypobaric hypoxia environment in treating pan-cancer.Scientific reports · 2025Article
- GFPT2 expression is induced by gemcitabine administration and enhances invasion by activating the hexosamine biosynthetic pathway in pancreatic cancer.Clinical & experimental metastasis · 2024Article
- Dose-Dependent Effect of Mitochondrial Superoxide Dismutase Gene Overexpression on Radioresistance of HEK293T Cells.International journal of molecular sciences · 2023Article
- Alteration in Levels of Specific miRNAs and Their Potential Protein Targets between Human Pancreatic Cancer Samples, Adjacent Normal Tissue, and Xenografts Derived from These Tumors.Life (Basel, Switzerland) · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Upregulation of CD73 Confers Acquired Radioresistance and is Required for Maintaining Irradiation-selected Pancreatic Cancer Cells in a Mesenchymal State.Molecular & cellular proteomics : MCP · 2020Article
- Inhibition of NF-κB-Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma.Cancer research · 2019Article
- Chemoresistance Transmission via Exosome-Mediated EphA2 Transfer in Pancreatic Cancer.Theranostics · 2018Article
- Superoxide Dismutases in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2017Review
- Analysis of Important Gene Ontology Terms and Biological Pathways Related to Pancreatic Cancer.BioMed research international · 2016Article
- The Relevance of Nrf2 Pathway and Autophagy in Pancreatic Cancer Cells upon Stimulation of Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2016Article
- Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer.Oxidative medicine and cellular longevity · 2016Review
- Article
- CDK1-Mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance.Molecular cancer therapeutics · 2015Article
- Comparative proteomic profiling of pancreatic ductal adenocarcinoma cell lines.Molecules and cells · 2014Article
- Plumbagin modulates leukemia cell redox status.Molecules (Basel, Switzerland) · 2014Article
- Redox-mediated and ionizing-radiation-induced inflammatory mediators in prostate cancer development and treatment.Antioxidants & redox signaling · 2014Review
- Comparing the metal concentration in the hair of cancer patients and healthy people living in the malwa region of punjab, India.Clinical Medicine Insights. Oncology · 2014Article
- Myeloprotection by cytidine deaminase gene transfer in antileukemic therapy.Neoplasia (New York, N.Y.) · 2013Review
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2 authors at 1 institution in 1 country.
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Abstract
Acquired resistance of cancer cells to anticancer drugs or ionizing radiation (IR) is one of the major obstacles in cancer treatment. Pancreatic cancer is an exceptional aggressive cancer, and acquired drug resistance in this cancer is common. Reactive oxygen species (ROS) play an essential role in cell apoptosis, which is a key mechanism by which radio- or chemotherapy induce cell killing. Mitochondria are the major source of ROS in cells. Thus, alterations in the expression of mitochondrial proteins, involved in ROS production or scavenging, may be closely linked to the resistance of cancer cells to radio- or chemotherapy. In the present study, we generated a stable cell line by exposing pancreatic cancer cells to increasing concentrations of ROS-inducing, anticancer compound 2-methoxyestradiol (2-ME) over a 3-month period. The resulting cell line showed strong resistance to 2-ME and contained an elevated level of ROS. We then used a comparative proteomics method to profile the differential expression of mitochondrial proteins between the parental and the resistant cells. One protein identified to be upregulated in the resistant cells was manganese superoxide dismutase (SOD2), a mitochondrial protein that converts superoxide radicals to hydrogen peroxides. Silencing of SOD2 resensitized the resistant cells to 2-ME, and overexpression of SOD2 led the parental cells to 2-ME resistance. In addition, the 2-ME-resistant cells also showed resistance to IR. Our results suggest that upregulation of SOD2 expression is an important mechanism by which pancreatic cancer cells acquire resistance to ROS-inducing, anticancer drugs, and potentially also to IR.
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