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Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

ABSTRACT: Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

PROVIDER: PRJNA743026 | ENA |

REPOSITORIES: ENA

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Transcriptomics analysis of KB-3-1 xenograft mice treated with cisplatin

Project description:This study was designed to evaluate the transcriptomic alterations mediated by cisplatin exposure in a human cancer xenograft mouse model. The tumor samples from xenograft mice with or without cisplatin treatment were applied to transcriptomic analysis.

2021-07-05 | GSE179263 | GEO

Integration of metabolomics and transcriptomics to reveal metabolic characteristics and key targets associated with cisplatin resistance in non-small cell lung cancer

Project description:Continuous exposure to cisplatin can induce drug resistance to limit efficacy, however, the underlying mechanisms correlated to cisplatin resistance are still unclear. Drug-sensitive A549 cells and cisplatin-resistant A549/DDP cells were used to explore the potential metabolic pathways and key targets associated with cisplatin resistance by integrating untargeted metabolomics with transcriptomics. The results of comprehensive analyses showed that 19 metabolites were significantly changed in A549/DDP vs A549 cells, and some pathways had a close relationship with cisplatin resistance, such as the biosynthesis of aminoacyl-tRNA, glycerophospholipid metabolism, and glutathione metabolism. Moreover, transcriptomics analysis showed glutathione metabolism was also obviously affected in A549/DDP, which indicated that glutathione metabolism played an import role in the process of drug resistance. Meanwhile, transcriptomics analysis suggested the four enzymes related to glutathione metabolism - CD13, GPX4, RRM2B, and OPLAH - as potential targets of cisplatin resistance in NSCLC. Further studies identified the over-expressions of these four enzymes in A549/DDP. The elucidation of mechanism and discovery of new potential targets may help us have a better understanding of cisplatin resistance.

2019-08-12 | PXD013265 | Pride

Transcriptomics analysis of Colon tumor xenograft model in streptozotocin-induced diabetic mice

Project description:This is a transcriptomics analysis contributing to a bigger project that tries to shed light on the role of type 2 diabetes mellitus (T2DM) as a risk factor for colon cancer (CC). Here we present a gene expression screening of 7 colon tumor xenograft samples, 2 with diabetic mice and 5 with normal blood glucose levels. For xenograft model details see: Prieto I, et al. (2017) Colon cancer modulation by a diabetic environment: A single institutional experience. PLoS One 12(3):e0172300

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Transcriptomics analysis of Colon tumor xenograft model in streptozotocin-induced diabetic mice

Project description:Transcriptomics analysis of Colon tumor xenograft model in streptozotocin-induced diabetic mice

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A transcriptomics approach identifies DR5-AS as a cisplatin-inducible long non-coding RNA that modulates cell cycle and proliferation

Project description:We have performed a transcriptomics study in which we first applied 80 uM of cisplatin for 16h. Total RNA was isolated from control as well as drug treated cells and apoptosis induction was confirmed by Annexin V and 7AAD staining. Total RNAs were subjected to deep-sequencing to identify differentially expressed RNAs. We then took advantage of bioinformatic tools to identify which lncRNAs are differentially expressed upon cisplatin treatment

2021-04-01 | GSE165560 | GEO

HMGB1 interactome in prostate and ovarian cancer cells treated with cisplatin

Project description:Cisplatin is used in chemotherapy of prostate, ovary and other cancer types but unfortunately the efficiency of cisplatin treatment is frequently hampered by acquired resistance. The cytotoxic effect of cisplatin has been attributed to its binding to DNA. HMGB1 is able to bind to cisplatin-DNA adducts with high affinity and its expression levels are associated with cisplatin resistance. This study reports the interactome of HMGB1 in prostate and ovarian cancer cells treated with cisplatin.

2021-11-01 | PXD026309 | Pride

Kidney inner medulla from mice treated with or without cisplatin

Project description:We are interested in the inner medulla of the kidney and how the nephrotoxic drug, cisplatin, may affect the transcriptome. Furthermore, we are interested in male and female inner medullary transcriptomic differences.

2023-01-01 | GSE195786 | GEO

Expression Data for Cisplatin Treated Dorsal Root Ganglia from A/J and C57BL/6J Mice

Project description:Peripheral sensory neuropathy is a common complication to cisplatin treatment in cancer patients. Multiple signaling pathways are likely to be implicated in the pathophysiology, there are no explicit treatments and little is known about predictive factors associated with the onset or progression of cisplatin induced peripheral neuropathy. The transcriptional profiles of differentially senesitive strains of dorsal root ganglion across two inbreed strain of mice will promote better understanding of progression and risk factors assocciated with cisplatin induced peripheral neuropathy. Peripheral neuropathy was induced with a bi-weekly treatment of 4mg/kg cisplatin. We used microarrays to detail the transciptional profile underlying cisplatin induced peirperal neuropathy in two differentailly sensitve inbreed strains of mice: A/J and C57BL/6J

2019-07-01 | GSE64174 | GEO

Transcription profiling by array of human A2780 ovarianc cancer cells and cisplatin resistant derivate cells treated with cisplatin or liposomal cisplatin

Project description:A2780 ovarian cancer cells and a cisplatin resistant derivate of A2780 cells, obtained from ECACC, UK, No. 93112519 [A2780] and No. 93112517 [A2780 cis] were seeded out in T-75 flasks at a density of 2x106 for A2780sens and 3x106 for A2780cis cells in 15 ml of medium and preincubated overnight. Medium was removed and 15 ml fresh medium (37M-0C) with different concentrations of cisplatin, liposomal cisplatin or empty liposomes were added and incubated for 72 h at 37M-0C in a 5% CO2 incubator. In case of A2780sens cells, 1.72 M-5M cisplatin (IC50 concentration) and in case of A2780cis cells 8.94 M-5M cisplatin (IC50 concentration) were added. Liposomal formulations contained equal cisplatin concentrations. Empty liposomes were added in the same concentration as the liposomal cisplatin, to analyze the impact of liposomal lipids (A2780sens: 0.80M-5mol lipid, A2780cis: 4.15 M-5mol lipid). After incubation, medium was removed and cells were washed thrice with 10 ml PBS. 1 ml RLT-buffer was added and cells lysates were stored at -80M-0C until RNA extraction.

2010-12-13 | E-MEXP-2840 | biostudies-arrayexpress

Expression data identifying hypermethylated genes associated with acquired cisplatin resistance

Project description:Treatment-related DNA hypermethylation may play a role in creating drug resistant phenotypes by inactivating genes that are required for cytotoxicity, but there have been no genome-wide studies to systematically investigate methylation of individual genes following exposure to chemotherapy. We used microarrays and a pharmacologic unmasking protocol in isogenic cisplatin-sensitive and -resistant cell lines to identify genes that were down-regulated in cisplatin-resistant cells and could be re-activated by the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-dC). We identified several hundred genes that were down-regulated in each resistant cell line. Of these, 30 genes were common to > 2 cell lines, and/or reported to be down-regulated in previous studies. siRNA knockdown of two candidate genes increased cell viability with cisplatin treatment in sensitive parental cell lines Cisplatin-sensitive and -resistant SCC cells and KB and KB cisplatin-resistant clones (n=2) were split to low density and treated with freshly prepared 5 microM 5-Aza-dC dissolved in 50% acetic acid/50% PBS or were mock treated with the same volume of vehicle in the media for 5 days. Subsequently, RNA was extracted and hybridized on Affymetrix U133A microarrays. Signal intensity and statistical significance was established for each transcript, and a 2-fold decrease in signal in each paired sensitive/resistant cell line in combination with 1.5-fold increase after 5Aza-dC treatment was used to identify candidate genes.

2010-04-12 | E-GEOD-19397 | biostudies-arrayexpress

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