Hypoxia is responsible for the altered response of ovarian cancer cells to the mitomycin C-drug
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PROVIDER: PRJNA1081461 | ENA |
REPOSITORIES: ENA
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Project description:Using HTA 2.0 microarrays, we demonstrate transcriptome changes in ovarian cancer SKOV3 cells induced by hypoxia, mitomycin C and their combined effect with particular emphasis on the effect of oxygen tension modification on mitomycin c activity. Examining differentially expressed genes (DEGs) in these groups.
2025-05-13 | GSE259424 | GEO
Project description:The environment inside even a small tumor is characterized by total (anoxia) or partial oxygen deprivation, hypoxia. It has been shown that radiotherapy and some conventional chemotherapies may be less effective in hypoxia, and therefore it is important to investigate how different drugs act in different microenvironments. In the associated study we performed a large screening of the effects of 19 clinically used or experimental chemotherapeutic drugs on four different cell lines in conditions of normoxia, hypoxia and anoxia. A panel of 19 commercially available drugs: 5-fluorouracil, acriflavine, bortezomib, cisplatin, digitoxin, digoxin, docetaxel, doxorubicin, etoposide, gemcitabine, irinotecan, melphalan, mitomycin c, rapamycin, sorafenib, thalidomide, tirapazamine, topotecan and vincristine were tested for cytotoxic activity on the cancer cell lines A2780 (ovarian), ACHN (renal), MCF-7 (breast), H69 (SCLC) and U-937 (lymphoma). Parallel aliquots of the cells were grown at different oxygen pressures and after 72 hours of drug exposure viability was measured with the fluorometric microculture cytotoxicity assay (FMCA). Sorafenib, irinotecan and docetaxel were in general more effective in an oxygenated environment, while cisplatin, mitomycin c and tirapazamine were more effective in a low oxygen environment. Surprisingly, hypoxia in H69 and MCF-7 cells mostly rendered higher drug sensitivity. In contrast ACHN appeared more sensitive to hypoxia, giving slower proliferating cells, and consequently, was more resistant to most drugs. Gene expression analysis was performed on MCF-7 cells after 90 hours in either anoxic or hypoxic conditions, and compared to cells grown in a regular cell incubator. The gene expression analysis was performed to validate that the cells were hypoxic/anoxic and showed the characteristic hypoxia response.
2014-05-04 | GSE47009 | GEO
Project description:The environment inside even a small tumor is characterized by total (anoxia) or partial oxygen deprivation, hypoxia. It has been shown that radiotherapy and some conventional chemotherapies may be less effective in hypoxia, and therefore it is important to investigate how different drugs act in different microenvironments. In the associated study we performed a large screening of the effects of 19 clinically used or experimental chemotherapeutic drugs on four different cell lines in conditions of normoxia, hypoxia and anoxia. A panel of 19 commercially available drugs: 5-fluorouracil, acriflavine, bortezomib, cisplatin, digitoxin, digoxin, docetaxel, doxorubicin, etoposide, gemcitabine, irinotecan, melphalan, mitomycin c, rapamycin, sorafenib, thalidomide, tirapazamine, topotecan and vincristine were tested for cytotoxic activity on the cancer cell lines A2780 (ovarian), ACHN (renal), MCF-7 (breast), H69 (SCLC) and U-937 (lymphoma). Parallel aliquots of the cells were grown at different oxygen pressures and after 72 hours of drug exposure viability was measured with the fluorometric microculture cytotoxicity assay (FMCA). Sorafenib, irinotecan and docetaxel were in general more effective in an oxygenated environment, while cisplatin, mitomycin c and tirapazamine were more effective in a low oxygen environment. Surprisingly, hypoxia in H69 and MCF-7 cells mostly rendered higher drug sensitivity. In contrast ACHN appeared more sensitive to hypoxia, giving slower proliferating cells, and consequently, was more resistant to most drugs. Gene expression analysis was performed on MCF-7 cells after 90 hours in either anoxic or hypoxic conditions, and compared to cells grown in a regular cell incubator. The gene expression analysis was performed to validate that the cells were hypoxic/anoxic and showed the characteristic hypoxia response. Microarray based mRNA profiling was used to charactarize cells grown in hypoxia and anoxia. In the associated study we performed a large screening of the effects of 19 clinically used or experimental chemotherapeutic drugs on four different cell lines in conditions of normoxia, hypoxia and anoxia. We fin that hypoxia/anoxia render cancer cells both more resistant and more sensistive, depending of the type of drug used. The gene expression analysis was performed to validate that the cells really were hypoxic/anoxic and showed the characteristic hypoxia response. The cell line used for the gene expression analysis was MCF-7.
2014-05-04 | E-GEOD-47009 | biostudies-arrayexpress
Project description:To dig out the synthetic lethality targets of mitomycin C, we we performed Genome-scale CRISPR-Cas9 knockout screening in SNU-1 with 0.1% DMSO or 0.3 µM MMC for 14 days. We found that BRCA2 is a synthetic lethality target of mitomycin C.
2022-06-08 | GSE132431 | GEO
Project description:Mouse lymphoma L5178Y cells are treated with Mitomycin C [CAS:50-07-7;CHEBI:27504] and harvested at 4 and 24 hours for analysis.
2004-05-13 | E-TOXM-8 | biostudies-arrayexpress
Project description:We showed that treatment with mitomycin C results in activation of an endonuclease that cleaves tRNAs in the anticodon loop. In an attempt to identify this nuclease, we performed RNA-seq on wild-type cells treated with and without mitomycin C. Differential gene expression was performed to identify genes expressed upon mitomycin C treatment.
2020-12-22 | GSE153782 | GEO
Project description:Mitomycin C is a DNA crosslinking agent. This experiment was carried out to determine the effect of Mitomycin C on genome wide transcription in Streptomyces venezuelae NRRL B65442.
2022-07-06 | E-MTAB-11556 | biostudies-arrayexpress
Project description:The goal of this study is to dig out how mitomycin C triggers apoptosis in the sensitive cells
2022-06-06 | GSE132327 | GEO
Project description:We have shown that mitomycin C induces expression of the rsr-yrlBA-rtcBA operon in Salmonella Typhimurium in a manner that is dependent on the activator for this operon, RtcR. As such, treatment with mitomycin C generates the ligand or other cellular conditions that activate RtcR and likely generates the substrates on which the components of this RNA repair operon act. We performed an RNA-seq analysis on WT cells and cells with components of the RNA repair operon, or the activator of the operon, deleted with and without mitomycin C. Changes in the transcriptome during mitomycin C between cells that do and do not express the RNA repair system were assessed.
2018-09-17 | GSE82167 | GEO
Project description:We performed RNASeq and confocal imaging analysis to characterize the gene expression changes in the cornea after wounding that modulate sensory axon integrity. We show that by preserving the ability of axons to attach to one another and to corneal epithelial cells, mitomycin C enhances sensory nerve recovery after mechanical injury.
2018-12-01 | GSE115355 | GEO