Effect of artemisinin on the expression of lung cancer related genes in mice with lung cancer
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE214362 | GEO | 2024/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:Effect of artemisinin on the expression of lung cancer related genes in mice with lung cancer
| PRJNA885068 | ENA
Project description:A cDNA microarray composed of 9065 uniEST probes was constructed and applied to detect the gene expression profile of protoscoleces of E. granulosus treated with albendazole and artemisinin in vitro, respectively. Compared with the untreated parasite, 7 genes were up-regulated and 38 genes were down-regulated in protoscoleces treated with albendazole and 100 genes were up-regulated and 6 genes were down-regulated in protoscoleces treated with artemisinin. The differential expression genes in protoscoleces induced by albendazole were clustered into energy metabolism, cell cycle and assembly of cell structure. And the differential expression genes affected by artemisinin were clustered into genetic information, the transduction of environmental signals, metabolism. Under transmission electron microscope observation, albendazole intervention damaged the cell structure, and form the heterochromatin in protoscoleces cells was mainly increased in the artemisinin group.
2014-06-03 | GSE58136 | GEO
Project description:We examined the antifungal activity of artemisinin against Aspergillus fumigatus (A. fumigatus), a pathogenic filamentous fungus responsible for allergic and invasive aspergillosis in humans and analyzed transcript profiles of the fungus on exposure to Artemisinin. A. fumigatus spores were cultured for 48 h and then treated with artemisinin (at MIC50 concentration) or solvent control (DMSO) for 3 h to study its transcriptomic profiles.
2011-05-11 | GSE21297 | GEO
Project description:A cDNA microarray composed of 9065 uniEST probes was constructed and applied to detect the gene expression profile of protoscoleces of E. granulosus treated with albendazole and artemisinin in vitro, respectively. Compared with the untreated parasite, 7 genes were up-regulated and 38 genes were down-regulated in protoscoleces treated with albendazole and 100 genes were up-regulated and 6 genes were down-regulated in protoscoleces treated with artemisinin. The differential expression genes in protoscoleces induced by albendazole were clustered into energy metabolism, cell cycle and assembly of cell structure. And the differential expression genes affected by artemisinin were clustered into genetic information, the transduction of environmental signals, metabolism. Under transmission electron microscope observation, albendazole intervention damaged the cell structure, and form the heterochromatin in protoscoleces cells was mainly increased in the artemisinin group. Isolated E. granulosus protoscoleces were treated with albendazole and artemisinin respectively and was extracted of total RNA using the TRIZOL Reagent according to the manufacturer's instructions. Gene-expression profiling was performed for each RNA sample separately on the GeneChip of Echinococcus granulosus Genome Array (Capitalbio) at CapitalBio Corporation (Beijing, China).
2014-06-03 | E-GEOD-58136 | biostudies-arrayexpress
Project description:The primary goal of toxicology and safety testing is to identify agents that have the potential to cause adverse effects in humans. Unfortunately, many of these tests have not changed significantly in the past 30 years and most are inefficient, costly, and rely heavily on the use of animals. The rodent cancer bioassay is one of these safety tests and was originally established as a screen to identify potential carcinogens that would be further analyzed in human epidemiological studies. Today, the rodent cancer bioassay has evolved into the primary means to determine the carcinogenic potential of a chemical and generate quantitative information on dose-response behavior in chemical risk assessments. Due to the resource-intensive nature of these studies, each bioassay costs $2 to $4 million and takes over three years to complete. Over the past 30 years, only 1,468 chemicals have been tested in a rodent cancer bioassay. By comparison, approximately 9,000 chemicals are used by industry in quantities greater than 10,000 lbs and nearly 90,000 chemicals have been inventoried by the U.S. Environmental Protection Agency as part of the Toxic Substances Control Act. Given the disparity between the number of chemicals tested in a rodent cancer bioassay and the number of chemicals used by industry, a more efficient and economical system of identifying chemical carcinogens needs to be developed. Experiment Overall Design: Five-week old female B6C3F1 mice were exposed for 13 weeks in the following dose groups: 1) 1,5-Naphthalenediamine, CAS No. 2243-62-1, feed, 2000 ppm, positive lung carcinogen; 2) 2,3-Benzofuran, CAS No. 271-89-6, gavage, 240 mg/kg, positive lung carcinogen; 3) 2,2-Bis(bromomethyl)-1,3-propanediol, CAS No. 3296-90-0, feed, 1250 ppm, positive lung carcinogen; 4) N-Methylolacrylamide, CAS No. 924-42-5, gavage (water), 50 mg/kg, positive lung carcinogen; 5) 1,2-Dibromoethane, CAS No. 106-93-4, gavage (corn oil), 62 mg/kg, positive lung carcinogen; 6) Coumarin, CAS No. 91-64-5, gavage (corn oil), 200 mg/kg, positive lung carcinogen; 7) Benzene, CAS No. 71-43-2, gavage (corn oil), 100 mg/kg, positive lung carcinogen; 8) N-(1-naphthyl)ethylenediamine dihydrochloride, CAS No. 1465-25-4, feed, 2000 ppm, negative lung carcinogen; 9) Pentachloronitrobenzene, CAS No. 82-68-8, feed, 8187 ppm, negative lung carcinogen; 10) 4-Nitroanthranilic acid, CAS No. 619-17-0, feed, 10000 ppm, negative lung carcinogen; 11) 2-Chloromethylpyridine hydrochloride, CAS No. 6959-47-3, gavage (water), 250 mg/kg, negative lung carcinogen; 12) Diazinon, CAS No. 333-41-5, feed, 200 ppm, negative lung carcinogen; 13) Malathion, CAS No. 121-75-5, feed, 16000 ppm, negative lung carcinogen; 14) Corn oil control, gavage; 15) Water control, gavage; 16) Rodent diet control, feed. Feed animals were exposed 7 days/week and gavage animals were exposed 5 days/week (5 ml/kg). After 13 weeks, animals were euthanized and lungs were collected. The right lobe was used for microarray analysis. Microarray analysis was performed on the lungs of three to four mice per treatment group.
2008-06-14 | E-GEOD-6116 | biostudies-arrayexpress
Project description:We examined the antifungal activity of artemisinin against Aspergillus fumigatus (A. fumigatus), a pathogenic filamentous fungus responsible for allergic and invasive aspergillosis in humans and analyzed transcript profiles of the fungus on exposure to Artemisinin. A. fumigatus spores were cultured for 48 h and then treated with artemisinin (at MIC50 concentration) or solvent control (DMSO) for 3 h to study its transcriptomic profiles. Total RNA (7 M-BM-5g) from A. fumigatus treated with solvent control (DMSO) or artemisinin was reverse transcribed separately using fluorescein-labeled dCTP or biotin-labeled dCTP from Micromax TSA labeling kit (Cy3 or Cy5 dyes are differentially deposited to these labeled cDNAs, post-hybridization, using tyramide signal amplification (TSA) protocol). Labeled cDNAs from test and control sample were mixed in equal amount and hybridized to microarray slide(s). After hybridization, the slides were processed as per the protocol of the Micromax TSA labeling kit and scanned in both the Cy3 and the Cy5 channels with a model 4200 Axon Instruments scanner with a 10-M-BM-5m resolution. Each of the signals was converted into a resolution of 16 bits per pixel. A dye swap experiment with a biological replicate was performed to ensure the reproducibility of each gene expression pattern.TIFF images were analyzed using GenePix Pro 6.0 software. The signal intensity value of each spot was reduced by the local background level for each spot. Diagnosis and normalization of microarray data (DNMAD) program was used for print-tip loess normalization of microarray data and for merging the data from dye-swap experiments . M-values obtained from this program were converted to log ratio (test/reference) and fold modulation. Genes having less than 3 spots in 2 dye swap slides were discarded and only those having their all fold change values (from 3 or 4 replicates in 2 slides; as each target is spotted twice on the slide) within a coefficient of variation M-BM-1 0.5 were used for analysis. Gene expression ratios of M-bM-^IM-%2 (fold upregulation or downregulation) in both replicates (dye swap) were considered to be differentially expressed genes.
2011-05-11 | E-GEOD-21297 | biostudies-arrayexpress
Project description:Plasmodium falciparum, the most pathogenic human malaria parasite, infects millions of human beings and causes a serious public health threat. Currently, the most potent anti-malarial drugs are artemisinin and its derivatives1,2. Artemisinin is a sesquiterpene lactone with an endoperoxide bridge3. The activation of artemisinin requires the cleavage of the endoperoxide bridge in the presence of iron sources4. Once activated, artemisinins are converted into highly reactive carbon-centered radicals5,6 that attack macromolecules through alkylation and propagate a series of damages, eventually leading to parasite death7,8. Even though several parasite proteins have been reported as the targets of artemisinin9,10, the exact mechanism of artemisinin action is still controversial and its high potency and specificity against the malaria parasite could not be fully accounted. Here, we have developed an unbiased chemical proteomics approach to directly probe the mechanism of action of artemisinin in P. falciparum in situ. An alkyne-tagged artemisinin analogue coupled with biotin enables selective purification and identification of 124 artemisinin covalent-binding protein targets, many of which are involved in essential biological processes of the parasite. In vitro assays confirm the specific artemisinin binding and inhibition of selected targets. Such a broad targeting spectrum disrupts the biochemical landscape of the parasite and causes its death. Furthermore, using the alkyne-tagged artemisinin coupled with a fluorescent dye to monitor its protein binding, we showed that heme, rather than free ferrous iron, is predominantly responsible for artemisinin activation. The extremely high level of heme released from the hemoglobin digestion by the parasite make artemisinin exceptionally potent against late-stage parasites (trophozoite and schizont stages) compared to parasites at early ring stage, which have low level of heme, mainly from endogenous synthesis. The ‘blood eating’ nature of the parasite with the release of large amounts of heme confers artemisinin with extremely high specificity against the parasites, with minimum side effects towards healthy red blood cells. Taken together, our results established a unifying model to explain the action and specificity of artemisinin in parasite killing. Our findings could facilitate the development of better alternative strategies to treat malaria in times of emerging artemisinin resistance11,12.
2015-12-17 | PXD002611 | Pride
Project description:This dataset pertains to a microarray-based transcriptomic profiling of artemisinin-resistant (6A-R, 11C-R) and artemisinin-sensitive (6A, 11C) P. falciparum under an an in vitro 4 hr artemisinin challenge (900nM), from 10 - 14 HPI
2018-03-22 | GSE112149 | GEO
Project description:The role of extracellular vesicles in developing artemisinin resistance in Plasmodium falciparum is not known. We have posited a role for EVs in the development of ARTr (EVs export hypothesis) (Tandoh et al.,2022).The objective of this study was to test a prediction of the EVs export hypothesis to gain insight into a putative role for EVs in the expression of the artemisinin resistant phenotype. We compared the gene expression profile of two artemisinin resistant parasites (C580R and R539T) generated by CRISPR based editing of an artemisinin susceptible parasite (Dd2) for enrichment with an EVs module of interest using gene set enrichment analysis.
2022-09-15 | GSE210644 | GEO
Project description:We sought to determine the transcriptomic impacts of artemisinin, Artemisia annua extract, and Artemisia afra extract on M. tuberculosis. Log phase cultures were treated with lethal doses for four hours or with inhibitory or sub-inhibitory doses for 24 hours. RNA was collected from untreated controls at the same timepoint.
2023-09-28 | GSE244235 | GEO