Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341276 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cisplatin is the first-line agent utilized for the clinical treatment of a wide variety of solid tumors including gastric cancer. However, the intrinsic or acquired cisplatin resistance is often occurred in patients with gastric cancer and resulted in failure of cisplatin therapy. In order to investigate if miRNA involves in cisplatin resistance of human gastric cancer, we first screened and compared the expression of miRNAs between cisplatin resistant gastric cancer cell lines SGC-7901/DDP and BGC-823/DDP and their sensitive parental cells by miRNAs microarray.
2016-09-05 | GSE86195 | GEO
Project description:microRNA profiling of gastric cancer vs. normal, pre-/-post CF (cisplatin/fluorouracil) chemotherapy. Biopsy samples were collected prior to chemotherapy from 90 gastric cancer patients treated with CF and from 34 healthy volunteers. At the time of disease progression, post-treatment samples were collected from 8 clinical responders. miRNA expression was determined using a custom-designed Agilent microarray. In order to identify an miRNA signature for chemotherapy resistance, we correlated miRNA expression levels with the time to progression (TTP) after CF. 90 pre-treatment gastric cancer samples, 34 healthy volunteers, 8 post-treatment samples.
2011-12-16 | E-GEOD-30070 | biostudies-arrayexpress
Project description:The development of chemo-resistance has dramatically limited the clinical efficiency of platinum-based therapy. Although many resistant mechanisms have been demonstrated, genetic/molecular alterations responsible for drug resistance in the majority of clinical cases has not been identified. We analyzed three pairs of testicular germ cell tumor (TGCT) cell lines using Affymetrix expression microarrays to identify differential expressed genes. Then the expression of CCND1/CyclinD1, selected from the microarray analysis, was determined in cisplatin sensitive and resistance cancer samples including TGCTs, ovarian and prostate cancers by quantitative reverse transcription PCR analysis (qRT-PCR). Finally, we determined the gene knocked-down effect of CyclinD1. Expression microarray study revealed a limited number of differentially expressed genes across all three cell lines when comparing the parental and resistant cells. Among them, CyclinD1 was the most significantly differentially expressed gene. Importantly, we found that, in clinical TGCT samples, the overall expression level of cyclinD1 is higher in resistant cases compared to those sensitive samples (9/12 in the resistant group and only 3/8 in the sensitive group). We also found that cyclinD1 expressed dozens of fold higher in the resistant than in the sensitive ovarian cancer cell lines and dramatically overexpressed in prostate cancer. We re-sensitized the resistant cells by knocking-down cyclinD1. We demonstrated that deregulation of cyclinD1 is the major cause of TGCT cisplatin resistance and it may also be commonly involved in other human cancers. Combined cyclinD1 inhibition and cisplatin chemotherapy may be used clinically to treat the large number of cyclinD1 deregulated resistant tumors. RNA from three paired parental and cisplatin-resistant TGCT cell lines was extracted and analysed by Affymetrix gene expression microarray profiling (Human Genome U133 plus 2.0 arrays). Expression changes associated with the resistant phenotype were identified by comparing the three cisplatin-resistant derivatives to their parental counterparts.
2010-03-15 | E-GEOD-14231 | biostudies-arrayexpress
Project description:Purpose: The goal of our study is to identify the differentially expressed genes between cispaltin sensitive and cisplatin resistance gastric cancer cell line. Methods: Transcriptome sequencing of cisplatin sensitive and cisplatin resistance KATOIII cells were generated by Illumina HiSeq TM, for triplicates Results : Using an optimized data analyzed workflow, we mapped 57773 genes and were found 5966 differentially expressed genes between cisplatin sensitive KATOIII and cisplatin resistance KATO/DDP cell lines.
2021-10-22 | GSE186205 | GEO
Project description:Cisplatin-resistant gastric cancer (GC) occurs in patients with GC treated with cisplatin-based chemotherapy, which results in disease progression and early recurrence during the treatment. To understand the initiation and developmental mechanism underlying cisplatin-resistant GC, we developed cisplatin resistant SGC7901 cells (SGC7901/DDP) from the parental cells (SGC7901/S) by continuous exposure to increasing concentrations of cisplatin and subjected these two cell lines to RNA sequencing analysis.
2019-04-17 | GSE122130 | GEO
Project description:Cisplatin is a broad-spectrum anticancer drug, which is estimated to be administered to 40-80% of patients undergoing chemotherapy. However, its clinical utility is often limited due to factors that include acquired resistance of cancer cells to cisplatin. Because cisplatin is currently evaluated as a prospective agent for combined chemotherapy of pancreatic ductal adenocarcinoma (PDAC), we have investigated mechanisms involved in the acquired resistance of PDAC cells to cisplatin using gene expression study of two different parental-resistant pairs of PDAC cell lines. We have developed cisplatin-resistant cell lines AsPC1-R and BxPC3-R from their parental PDAC cell lines AsPC1 and BxPC3, respectively, by culturing them in medium with step-wise increasing concentration of cisplatin. Parental and resistant pairs of PDAC cells were analyzed by whole-transcript gene expression analysis.
2015-11-30 | GSE73978 | GEO
Project description:microRNA profiling of gastric cancer vs. normal, pre-/-post CF (cisplatin/fluorouracil) chemotherapy. Biopsy samples were collected prior to chemotherapy from 90 gastric cancer patients treated with CF and from 34 healthy volunteers. At the time of disease progression, post-treatment samples were collected from 8 clinical responders. miRNA expression was determined using a custom-designed Agilent microarray. In order to identify an miRNA signature for chemotherapy resistance, we correlated miRNA expression levels with the time to progression (TTP) after CF.
2011-12-16 | GSE30070 | GEO
Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.
2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress
Project description:Platinum-based chemotherapeutics are used in many combination regimens in cancer. Despite extensive use across diverse cancer types, there is room for improved efficacy and patient selection for treatment. Here, we use bladder cancer to address both issues. A multi-omic assessment of five human bladder cancer cell lines and their chemotherapy resistant derivatives, coupled with in vitro whole-genome CRISPR screens were used to define functional drivers of treatment resistance. We identified 46 genes that sensitized the resistant cell lines to cisplatin plus gemcitabine (GemCis), a standard combination therapy in bladder cancer. Most genes were involved with DNA damage and repair pathways, which have previously been associated with enhanced sensitivity to cisplatin. Evaluating expression of the 46 genes in the whole transcriptome and proteome data in parental and resistant lines identified the puromycin sensitive aminopeptidase, NPEPPS, as a novel hit. Depletion of NPEPPS resulted in sensitizing resistant bladder cancer cells to cisplatin in vitro and in xenograft experiments. Pharmacologic inhibition of NPEPPS with tosedostat in cells and in chemoresistant, bladder cancer patient-derived tumoroids improved response to cisplatin. Prior work found NPEPPS in a protein complex with volume regulated anion channels (VRACs) in several cell line models. Interestingly, depletion of two VRAC subunits, LRRC8A and LRRC8D, known importers of intracellular cisplatin, enhanced resistance to cisplatin. Our findings support NPEPPS as a novel and druggable driver of cisplatin resistance with the potential for rapid translation to clinical investigation.
2024-02-20 | PXD024742 | Pride
Project description:Cisplatin-resistance is a major cause of treatment failure in human ovarian cancer. Besides lots of genes involved, emerging evidences demonstrate that miRNAs contribute to cisplatin-resistance in cancer. We measured the miRNA expression profiles of cisplatin-resistant C13K ovarian cancer cell line compared with its cisplatin-sensitive OV2008 parent cell line using miRNA microarrays.
2018-09-28 | GSE120256 | GEO