ArticleMedical oncology (Northwood, London, England)2012
Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase.
Article in Medical oncology (Northwood, London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- N-acetylcysteine attenuates sodium arsenite-induced oxidative stress and apoptosis in embryonic fibroblast cells.Toxicology research · 2024Article
- The p53-mediated cell cycle regulation is a potential mechanism for emodin-suppressing osteosarcoma cells.Heliyon · 2024Article
- Bioinformatics integrated analysis to investigate candidate biomarkers and associated metabolites in osteosarcoma.Journal of orthopaedic surgery and research · 2021Article
- Integrated Analysis of DEAD-Box Helicase 56: A Potential Oncogene in Osteosarcoma.Frontiers in bioengineering and biotechnology · 2020Article
- Reprogramming factors induce proliferation and inhibit apoptosis of melanoma cells by changing the expression of particular genes.Molecular medicine reports · 2019Article
- Protective effects of mitochondrion-targeted peptide SS-31 against hind limb ischemia-reperfusion injury.Journal of physiology and biochemistry · 2018Article
- Catalase down-regulation in cancer cells exposed to arsenic trioxide is involved in their increased sensitivity to a pro-oxidant treatment.Cancer cell international · 2018Article
- Electrozymographic evaluation of the attenuation of arsenic induced degradation of hepatic SOD, catalase in an in vitro assay system by pectic polysaccharides ofBiochemistry and biophysics reports · 2017Article
- Reprogramming Factors Remodel Melanoma Cell Phenotype by Changing Stat3 Expression.International journal of medical sciences · 2017Article
- Differential transcriptional regulation of hypoxia-inducible factor-1α by arsenite under normoxia and hypoxia: involvement of Nrf2.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Resveratrol protects against arsenic trioxide-induced oxidative damage through maintenance of glutathione homeostasis and inhibition of apoptotic progression.Environmental and molecular mutagenesis · 2015Article
- Arsenic Trioxide Activate Transcription of Heme Oxygenase-1 by Promoting Nuclear Translocation of NFE2L2.International journal of medical sciences · 2015Article
- Heme oxygenase-1 silencing increases the sensitivity of human osteosarcoma MG63 cells to arsenic trioxide.Molecular and cellular biochemistry · 2014Article
- Combinative effects of thanh hao miet giap thang (sweet wormwood and tortoise shell decoction) ingredients on antioxidative activity in vitro.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2014Article
- Silencing SATB1 inhibits the malignant phenotype and increases sensitivity of human osteosarcoma U2OS cells to arsenic trioxide.International journal of medical sciences · 2014Article
- Silencing SATB1 inhibits proliferation of human osteosarcoma U2OS cells.Molecular and cellular biochemistry · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect. Apoptotic cells were detected by flow cytometry with Annexin-V-FITC/PI dual staining. Intracellular ROS was measured by flow cytometry using a cell-based ROS assay kit. Catalase activity and mRNAs were analyzed by ELISA and real-time qRT-PCR, respectively. Apoptosis and intracellular ROS of MG63 cells increased in a dose-dependent manner following arsenic treatments. Both were prevented by the presence of the anti-oxidative reagent N-acetyl-L: -cysteine (NAC) or catalase (CAT). Furthermore, the activity and mRNA of catalase were decreased strikingly following arsenic exposure. The present study indicates that p53 null osteosarcoma MG63 cells are susceptible to the ATO; the inhibition of catalase and the resulted intracellular ROS accumulation are an important molecular mechanism under which ATO induces apoptosis of p53-deficient osteosarcoma cells.
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