ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Reactive oxygen species mediate oxaliplatin-induced epithelial-mesenchymal transition and invasive potential in colon cancer.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Prognostic Value of Peroxiredoxin-1 Expression in Patients with Solid Tumors: a Meta-Analysis of Cohort Study.Disease markers · 2021Pooled it
- Systematic review of the old and new concepts in the epithelial-mesenchymal transition of colorectal cancer.World journal of gastroenterology · 2016Pooled it
- Analysis of the Prognostic Potential of Schlafen 11, Programmed Death Ligand 1, and Redox Status in Colorectal Cancer Patients.International journal of molecular sciences · 2023Article
- Natural Compound Shikonin Induces Apoptosis and Attenuates Epithelial to Mesenchymal Transition in Radiation-Resistant Human Colon Cancer Cells.Biomolecules & therapeutics · 2022Article
- Environmental Risk Assessment of Oxaliplatin Exposure on Early Life Stages of Zebrafish (Toxics · 2022Article
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- Platinum-Based Drugs Cause Mitochondrial Dysfunction in Cultured Dorsal Root Ganglion Neurons.International journal of molecular sciences · 2020Article
- The Role of Oxidative Stress and Its Counteractive Utility in Colorectal Cancer (CRC).Cancers · 2020Review
- Advances in Understanding TKS4 and TKS5: Molecular Scaffolds Regulating Cellular Processes from Podosome and Invadopodium Formation to Differentiation and Tissue Homeostasis.International journal of molecular sciences · 2020Review
- Dual roles of chromatin remodeling protein BRG1 in angiotensin II-induced endothelial-mesenchymal transition.Cell death & disease · 2020Article
- Article
- Redox-Mediated Mechanism of Chemoresistance in Cancer Cells.Antioxidants (Basel, Switzerland) · 2019Review
- Non-redundant functions of EMT transcription factors.Nature cell biology · 2019Review
- Salidroside improves the hypoxic tumor microenvironment and reverses the drug resistance of platinum drugs via HIF-1α signaling pathway.EBioMedicine · 2018Article
- DUOX2-mediated production of reactive oxygen species induces epithelial mesenchymal transition in 5-fluorouracil resistant human colon cancer cells.Redox biology · 2018Article
- Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer.Oxidative medicine and cellular longevity · 2018Article
- Dihydroartemisinin inhibits EMT induced by platinum-based drugs via Akt-Snail pathway.Oncotarget · 2017Article
- EMT and inflammation: inseparable actors of cancer progression.Molecular oncology · 2017Review
- Metabolic shift toward oxidative phosphorylation in docetaxel resistant prostate cancer cells.Oncotarget · 2016Article
- Peroxiredoxin V Inhibits Emodin-induced Gastric Cancer Cell ApoptosisIn vivo (Athens, Greece)Article
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
Therapeutic benefits offered by common chemotherapy drugs, such as oxaliplatin, are limited due to the development of resistance, which contributes to treatment failure and metastasis. The epithelial-mesenchymal transition (EMT) is a key event contributing to the development of resistance to chemotherapeutics. Although the relationship between oxaliplatin and chemotherapy resistance has been described for decades, the molecular mechanisms have remained elusive. The aim of the present study was to investigate the underlying mechanisms of oxaliplatin-mediated metastasis. Here, we identify reactive oxygen species (ROS) as mediators that promote the oxaliplatin-induced EMT. Following oxaliplatin treatment, the messenger RNA (mRNA) levels of most peroxiredoxin family genes, except for peroxiredoxin 1 (prdx1) gene, were constant or even decreased, resulting in ROS abundance. And the antioxidant guardian Nrf2 was unconspicuously raised both transcriptionally and translationally with oxaliplatin treatment as compared to those induced by topotecan treatment, which has been proved with no induced metastasis. In addition, the study evaluated high levels of ROS leading to EMT via activation of the known oncogenes Akt and Snail. Using the Akt inhibitor LY294002 or knocking down Snail expression via RNA interference (RNAi) reversed the effects of oxaliplatin on the EMT and metastasis. Our studies establish a role for the ROS-Akt-Snail axis as a mechanism by which chemotherapeutics induce EMT and cancer metastasis.
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