Project description:RNA sequencing data of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. Samples include 7 parental and 10 derived resistant cell lines. Our aim was to assess whether the resistant cells had undergone Epithelial to Mesenchymal Transition upon resistance acquisition.
Project description:Genome wide DNA methylation profiling of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. The Illumina Infinium 450k and EPIC Human DNA methylation Beadchips were used to obtain DNA methylation profiles across approximately 450,000 or 850,000 CpGs from the cells. Samples include 7 parental and 10 derived resistant cell lines.
Project description:Genome wide DNA methylation profiling of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. Followig the published TAB-sequencing protocol, the Illumina Infinium 450K or EPIC Human DNA methylation Beadchips were used to obtain DNA hydroxymethylation profiles across approximately 450,000 or 850,000 CpGs from the cells. Samples include 5 parental and 6 derived resistant cell lines.
Project description:RNA sequencing data of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. Samples include 7 parental and 10 derived resistant cell lines. Our aim was to assess whether the resistant cells had undergone Epithelial to Mesenchymal Transition upon resistance acquisition and whether EMT disappears upon knock down of the DNMTs
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.
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.
Project description:microRNA and mRNA profiling was conducted for parental cell lines and cell lines resistant to trifluridine in 3 colorectal cell lines (DLD-1, HCT-116, RKO). We hypothesized that a detailed comparison between miRNA and mRNA expression might reveal the mechanism for acquired resistant to trifluridine in colorectal cancer.
Project description:microRNA and mRNA profiling was conducted for parental cell lines and cell lines resistant to trifluridine in 3 colorectal cell lines (DLD-1, HCT-116, RKO). We hypothesized that a detailed comparison between miRNA and mRNA expression might reveal the mechanism for acquired resistant to trifluridine in colorectal cancer.