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272 results on '"Kassie, Fekadu"'

11. Inhibition of lung adenocarcinoma by combinations of sulfasalazine (SAS) and disulfiram-copper (DSF-Cu) in cell line models and mice.

Author

Bagherpoor, Alireza Jian, Shameem, Mohammad, Luo, Xianghua, Seelig, Davis, and Kassie, Fekadu

Subjects
NON-small-cell lung carcinoma, REACTIVE oxygen species, CELL lines, ANIMAL disease models, LABORATORY mice
Abstract

Sulfasalazine (SAS) is a repurposed antitumor drug which inhibits the proliferation and survival of cancer cells by inhibiting the xCT cellular antioxidant system. Recent clinical studies have shown that, due to poor bioavailability, the antitumor effects of SAS monotherapy are minimal. Therefore, we hypothesized that DSF, another repurposed drug that has demonstrated anticancer effects, or its complex with copper (DSF-copper, DSF-Cu) could potentiate the antilung cancer effects of SAS. Exposure of non-small cell lung cancer cells to therapeutically achievable concentrations of SAS-induced low-to-moderate cytotoxic effects (20–40% reduction in cell viability) and, unexpectedly, induced the antioxidant protein NRF2 and its downstream effectors xCT and ALDH1A1. However, combinations of SAS and DSF-Cu, but not SAS and DSF, induced a significantly higher cytotoxic effect (64–88% reduction in cell viability), apoptosis and generation of mitochondrial reactive oxygen species as compared with SAS or DSF-Cu alone. Moreover, DSF-Cu abrogated SAS-induced NRF2, xCT and ALDH1A1 expression. In a mouse model of lung tumor, SAS + DSF-Cu showed a higher efficacy than the individual drugs in reducing the number and size of tumors as well as the incidence and multiplicity of lung adenocarcinoma. Taken together, our findings indicate that the observed antilung cancer effects of SAS plus DSF-Cu are mediated, at least in part, via impairment of reactive oxygen species defense and -enhancement of oxidative stress and provide evidence for the preventive/therapeutic potential of this combinatorial approach against lung cancer. [ABSTRACT FROM AUTHOR]

Published
2023
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16. The production of reactive oxygen species and the mitochondrial membrane potential are modulated during onion oil-induced cell cycle arrest and apoptosis in A549 cells

Author

Wu, Xin-jiang, Stahl, Thorsten, Hu, Ying, Kassie, Fekadu, and Mersch-Sundermann, Volker

Subjects
Allium -- Nutritional aspects, Allium -- Research, Onions -- Nutritional aspects, Onions -- Research, Cell cycle -- Research, Apoptosis -- Research, Cancer -- Prevention, Cancer -- Research, Food/cooking/nutrition
Abstract

Protective effects of Allium vegetables against cancers have been shown extensively in experimental animals and epidemiologic studies. We investigated cell proliferation and the induction of apoptosis by onion oil extracted from Allium cepa, a widely consumed Allium vegetable, in human lung cancer A549 cells. GC/MS analysis suggested that propyl sulfides but not allyl sulfides are major sulfur-containing constituents of onion oil. Onion oil at 12.5 mg/L significantly induced apoptosis (13% increase of apoptotic cells) as indicated by sub-G1 DNA content. It also caused cell cycle arrest at the G2/M phase; 25 mg/L onion oil increased the percentage of G2/M cells almost 6-fold compared with the dimethyl sulfoxide control. The action of onion oil may occur via a reactive oxygen species-dependent pathway because cell cycle arrest and apoptosis were blocked by the antioxidants N-acetylcysteine and exogenous glutathione. Marked collapse of the mitochondrial membrane potential suggested that dysfunction of the mitochondria may be involved in the oxidative burst and apoptosis induced by onion oil. Expression of phospho-cdc2 and phospho-cyclin B1 were downregulated by onion oil, perhaps accounting for the G2/M arrest. Overall, these results suggest that onion oil may exert chemopreventive action by inducing cell cycle arrest and apoptosis in tumor cells. KEY WORDS: * onion * allium * cell cycle * apoptosis * chemoprevention

Published
2006

27. Genotoxic and ecotoxic effects of groundwaters and their relation to routinely measured chemical parameters

Author

Helma, Christoph, Eckl, Peter, Gottmann, Eva, Kassie, Fekadu, Rodinger, Wolfgang, Steinkellner, Hans, Windpassinger, Christian, Schulte-Hermann, Rolf, and Knasmuller, Siegfried

Subjects
Aquifers -- Testing, Water quality management -- Testing, Environmental monitoring -- Measurement, Environmental issues, Science and technology
Abstract

An investigation into the genotoxic and ecotoxic effects of groundwater was correlated with the physical and chemical characteristics of the groundwater sample. Results of the correlations showed that the physical and chemical parameters tested did not indicate the potential genotoxic or ecotoxic potential of the tested groundwater, necessitating the addition of biological toxicity testing to improve the efficacy of groundwater testing programs.

Published
1998

29. Diet and DNA Damage

Author

Knasmüller, Siegfried, primary, Kassie, Fekadu, additional, Steinkellner, Hans, additional, Hietsch, Gerhard, additional, and Huber, Wolfgang, additional

Published
2000
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31. Comparative evaluation of four bacterial assays for the detection of genotoxic effects in the dissolved water phases of aqueous matrices

Author

Helma, Christoph, Mersch-Sundermann, Volker, Houk, Virginia S., Glasbrenner, Ursula, Klein, Carmen, Wenquing, Lu, Kassie, Fekadu, Schulte-Hermann, Rolf, and Knasmuller, Siegfried

Subjects
Microbiological assay -- Evaluation, Genetic toxicology -- Research, Environmental issues, Science and technology
Abstract

A study was conducted on four bacterial genotoxicity assays recommended for screening large sample numbers, namely, Salmonella/microsome assay, SOS Chromotest, Microscreen phage-induction assay and differential DNA repair test. The assays are being eyed for several environmental applications. SOS Chromotest showed to be the most efficient for routine screening of water samples.

Published
1996

47. Transcriptome profiling in oral cavity and esophagus tissues from (S)-N′-nitrosonornicotine-treated rats reveals candidate genes involved in human oral cavity and esophageal carcinogenesis

Author

Khammanivong, Ali, Anandharaj, Arunkumar, Qian, Xuemin, Song, Jung Min, Upadhyaya, Pramod, Balbo, Silvia, Bandyopadhyay, Dipankar, Dickerson, Erin B., Hecht, Stephen S, and Kassie, Fekadu

Subjects
Male, Mouth, Nitrosamines, Esophageal Neoplasms, Carcinogenesis, Article, Rats, Inbred F344, Gene Expression Regulation, Neoplastic, Esophagus, Carcinogens, Animals, Humans, Mouth Neoplasms, Transcriptome
Abstract

Recently, we have shown that (S)-N'-Nitrosonornicotine [(S)-NNN], the major form of NNN in tobacco products, is a potent oral cavity and esophageal carcinogen in rats. To determine the early molecular alterations induced by (S)-NNN in the oral and esophageal mucosa, we administered the carcinogen to rats in the drinking water for 10 wk and global gene expression alterations were analyzed by RNA sequencing. At a false discovery rate P-value 0.05 and fold-change ≥2, we found alterations in the level of 39 genes in the oral cavity and 69 genes in the esophagus. Validation of RNA sequencing results by qRT-PCR assays revealed a high cross-platform concordance. The most significant impact of exposure to (S)-NNN was alteration of genes involved in immune regulation (Aire, Ctla4, and CD80), inflammation (Ephx2 and Inpp5d) and cancer (Cdkn2a, Dhh, Fetub B, Inpp5d, Ly6E, Nr1d1, and Wnt6). Consistent with the findings in rat tissues, most of the genes were deregulated, albeit to different degrees, in immortalized oral keratinocytes treated with (S)-NNN and in non-treated premalignant oral cells and malignant oral and head and neck squamous cells. Furthermore, interrogation of TCGA data sets showed that genes deregulated by (S)-NNN in rat tissues (Fetub, Ly6e, Nr1d1, Cacna1c, Cd80, and Dgkg) are also altered in esophageal and head and neck tumors. Overall, our findings provide novel insights into early molecular changes induced by (S)-NNN and, therefore, could contribute to the development of biomarkers for the early detection and prevention of (S)-NNN-associated oral and esophageal cancers. © 2016 Wiley Periodicals, Inc.

Published
2016

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