ArticleAntioxidants & redox signaling2009
Different redox states in malignant and nonmalignant esophageal epithelial cells and differential cytotoxic responses to bile acid and honokiol.
Article in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Modulation of the oxidative plasmatic state in gastroesophageal reflux disease with the addition of rich water molecular hydrogen: A new biological vision.Journal of cellular and molecular medicine · 2018Trial
- A redox probe screens MTHFD1 as a determinant of gemcitabine chemoresistance in cholangiocarcinoma.Cell death discovery · 2021Article
- Review
- Honokiol induces reactive oxygen species-mediated apoptosis in Candida albicans through mitochondrial dysfunction.PloS one · 2017Article
- Article
- Overproduction of reactive oxygen species - obligatory or not for induction of apoptosis by anticancer drugs.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2016Article
- Cyclophilin 40 alters UVA-induced apoptosis and mitochondrial ROS generation in keratinocytes.Experimental cell research · 2013Article
- Warburg and Crabtree effects in premalignant Barrett's esophagus cell lines with active mitochondria.PloS one · 2013Article
- Single-cell analysis reveals early manifestation of cancerous phenotype in pre-malignant esophageal cells.PloS one · 2013Article
- Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- A novel synthetic C-1 analogue of 7-deoxypancratistatin induces apoptosis in p53 positive and negative human colorectal cancer cells by targeting the mitochondria: enhancement of activity by tamoxifen.Investigational new drugs · 2012Article
- Preferential killing of cancer cells with mitochondrial dysfunction by natural compounds.Mitochondrion · 2010Review
- Small mitochondria-targeting molecules as anti-cancer agents.Molecular aspects of medicine · 2010Review
- Conventional Western Treatment Associated With Chinese Herbal Medicine Ameliorates the Incidence of Head and Neck Cancer Among Patients With Esophageal Cancer.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Esophageal adenocarcinoma (EAC) is a highly lethal cancer in western countries. EAC cells are believed to develop from esophageal epithelial cells through complex transformation processes involving inflammation and oxidative stress. The purpose of this study was to compare the redox status of malignant and nonmalignant esophageal epithelial cells and to test their responses to bile acid-induced oxidative stress and to treatment with honokiol (HNK), a natural product with anticancer activity. We demonstrated that esophageal adenocarcinoma cells express significantly higher levels of antioxidant molecules and were resistant to reactive oxygen species (ROS) stress induced by bile acid, but were sensitive to the cytotoxic action of HNK. Mechanistic study showed that HNK caused cancer cell death by disruption of mitochondrial transmembrane potential and was correlated with cyclophilin D (CypD) expression. Inhibition of CypD by cyclosporin A or abrogation of its expression by siRNA significantly suppressed the cytotoxicity of HNK, suggesting that CypD may be a key molecule that mediates the cytotoxicity. Our study suggests that the high antioxidant capacity in EAC cells confers on them the ability to survive the oxidative microenvironment in the reflux esophagus, and that HNK is a promising compound to kill the transformed cells preferentially.
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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.