ArticleCancer cell international2011
In vitro effects of 2-methoxyestradiol-bis-sulphamate on reactive oxygen species and possible apoptosis induction in a breast adenocarcinoma cell line.
Article in Cancer cell international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2023Review
- Dysregulation of Catalase by a Sulphamoylated Estradiol Analogue Culminates in Antimitotic Activity and Cell Death Induction in Breast Cancer Cell Lines.Molecules (Basel, Switzerland) · 2021Article
- Sulphamoylated Estradiol Analogue Induces Reactive Oxygen Species Generation to Exert Its Antiproliferative Activity in Breast Cancer Cell Lines.Molecules (Basel, Switzerland) · 2020Article
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- In vitro assessment of a computer-designed potential anticancer agent in cervical cancer cells.Biological research · 2016Article
- Effects of 2-methoxyestradiol on apoptosis and HIF-1α and HIF-2α expression in lung cancer cells under normoxia and hypoxia.Oncology reports · 2016Article
- Hyperoxia-induced changes in estradiol metabolism in postnatal airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Novel estradiol analogue induces apoptosis and autophagy in esophageal carcinoma cells.Cellular & molecular biology letters · 2014Article
- Induction of the intrinsic apoptotic pathway via a new antimitotic agent in an esophageal carcinoma cell line.Cell & bioscience · 2014Article
- An estrogen analogue and promising anticancer agent refrains from inducing morphological damage and reactive oxygen species generation in erythrocytes, fibrin and platelets: a pilot study.Cancer cell international · 2014Article
- Molecular crosstalk between apoptosis and autophagy induced by a novel 2-methoxyestradiol analogue in cervical adenocarcinoma cells.Cancer cell international · 2013Article
- 2-Methoxyestradiol-bis-sulphamate refrains from inducing apoptosis and autophagy in a non-tumorigenic breast cell line.Cancer cell international · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the search for anticancer agents, a promising 17-β-estradiol metabolite, 2-methoxyestradiol (2ME2) was found that exerts antiproliferative in vitro and in vivo activity. Since 2ME2 has limited biological accessibility and rapid metabolic degradation, the purpose of this study was to investigate the in vitro influence exerted by an analogue of 2ME2 namely 2-methoxyestradiol-bis-sulphamate (2MEBM) in a breast adenocarcinoma cell line (MCF-7).
methodsThis was conducted by investigating 2MEBM's in vitro influence on cell cycle progression, mitochondrial membrane potential and possible production of reactive oxygen species (ROS) generation. In vitro effects of 2MEBM on cell cycle progression was demonstrated by means of flow cytometry using propidium iodide. Hydrogen peroxide and superoxide production was investigated using 2,7-dichlorofluorescein diacetate and hydroethidine, respectively. The probable reduction in the mitochondrial membrane potential was demonstrated using a MitoCapture™ kit.
resultsCell cycle progression revealed the presence of a sub-G1 apoptotic peak. Reduction of mitochondrial membrane potential after exposure to 2MEBM was demonstrated and an increase in ROS production was also observed.
conclusionThis study verified that 2MEBM exposure resulted in apoptosis induction, increased ROS production and reduced mitochondrial membrane potential in a tumorigenic breast epithelial cell line. Data obtained from this project contributes to the unravelling of the in vitro signal transduction of 2MEBM in tumorigenic cell lines.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.