5-FU resistant ESCC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE69494 | GEO | 2015/06/03
SECONDARY ACCESSION(S): PRJNA285737
REPOSITORIES: GEO
Similar Datasets
Project description:The transcriptional profiles of the HCT116 parental cells following treatment with either 5-FU or SN38 for 24h were assessed. In addition, basal comparisons between HCT116 parental and HCT116 5-FU -resistant and HCT116 SN38-resistant cells were also assessed.
2009-03-30 | E-MEXP-1691 | biostudies-arrayexpress
Project description:Copy number profiling of MKN45T 5-FU resistant gastric cancer cell lines and its parental cell line MKN45. We hypothesized that a detailed fine-scale survey of genomic CNAs might reveal the mechanism for acquired resistant to 5-FU in gastric cancer.
2017-06-09 | GSE89191 | GEO
Project description:In the present study, we investigated miRNA expression changes caused by aquired chemoresistance to 5-FU or Oxa. 40 and 14 miRNAs were detected as differentially expressed in 5-fluouracil- and oxaliplatin-resistant colorectal HCT116 sublines, respectively. Differentially expressed miRNAs determined in the present study could be applied for further development of diagnostic and therapeutic applications for colorectal cancer carcinoma resistant to 5-FU or Oxa.
2019-12-31 | GSE119481 | GEO
Project description:Parental and 5-fluorouracil (5-FU)-resistant HCT15 cells were treated with 5-FU or vehicle for 12h and assembled into an IMPRINTS-CETSA scheme with 6 different heating temperatures (37ºC, 47ºC, 50ºC, 52ºC, 54ºC, and 57ºC) with each set of samples heated at one temperature included in the same isobaric TMT10 set and measured at the same time on the mass spectrometer.
This entry contains two datasets:
1. 5-FU in parental vs. resistant HCT15 (file names “12h 5FU_par vs resHCT15”) for data referred to as HCT15_Par_5FU and HCT15_Res_5FU in the associated publication. The labelling order of samples in the TMT10 channels for this dataset was as follows: 37C/47C/50C/52C/54C/57C samples: Biorep1_Parental_Vehicle (126), Biorep1_Parental_5FU_100µM (127N), Biorep1_Resistant_5FU_16µM (127C), Biorep2_ Parental_Vehicle (128N), Biorep2_ Parental_5FU_100µM (128C), Biorep2_ Resistant_5FU_16µM (129N), Biorep3_ Parental_Vehicle (129C), Biorep3_ Parental_5FU_100µM (130N), Biorep3_ Resistant_5FU_16µM (130C), mixed_control (131).
2. 5-FU in resistant HCT15 (file names “12h 5FU_ResHCT15_diff”) for data referred to as HCT15_Res_Diff in the in the associated publication. The labelling order of samples in the TMT10 channels for this dataset was as follows: 37C/47C/50C/52C/54C/57C samples: Biorep1_ Resistant_5FU_16µM (128N), Biorep2_ Resistant_5FU_16µM (128C), Biorep3_ Resistant_5FU_16µM (129N), Biorep1_ Resistant_5FU_100µM (129C), Biorep2_ Resistant_5FU_100µM (130N), Biorep3_ Resistant_5FU_100µM (130C), mixed_control (131).
For additional details see the methods section of the associated publication.
2021-07-15 | PXD026472 | JPOST Repository
Project description:5-Fluorouracil (5-FU) is one of the most common drugs used in chemotherapy because of its efficacy and stability. However, 5-FU has been known to work on only 10~15% of colon cancer patients. Therefore, the study of 5-FU sensitivity study is necessary to increase the survival of colon cancer patients. p53 is one of the factors that effect on drug sensitivity. Main function of p53 has been focused on transcription activity in cell death. Numerous drug related studies show that expression of wild-type p53 increases drug sensitivity in various cancer types through inducing apoptotic signaling pathways. Currently, it has been reported that p53 has both transcriptional and non-transcriptional activities in apoptosis. However, most studies about p53 non-transcriptional activities in apoptosis are mainly focused on p53 induced mitochondrial outer membrane permeabilization, triggering the release of pro-apoptotic factors. The chromatin structure and organization have strongly attracted because of their impacts in cellular phenotypes. Recent studies have been shown that changes in chromatin accessibility affect cell phenotypes for external stimuli. Since p53 plays an important role in drug sensitivity and 5-FU is an external stimulus for cancer cells, we hypothesized that p53 may effect on 5-FU sensitivity through different regulation of chromatin accessible regions between TP53-WT and TP53-KO cells. To determine the effect of p53 on chromatin accessibility modification associated with 5-FU sensitivity, ATAC-seq and RNA-seq were performed under 5-FU treatment on TP53-WT as drug sensitive and TP53-KO as drug resistant HCT116 cells. In this study, we found that 5-FU induces chromatin accessibility in both TP53-WT and TP53-KO cells. Moreover, our results show that 5-FU induced chromatin accessibility increases expression of apoptotic genes in TP53-WT HCT116 cells through p53 non-transcriptional activity in nucleus.
2021-02-10 | GSE157950 | GEO
Project description:5-Fluorouracil (5-FU) is one of the most common drugs used in chemotherapy because of its efficacy and stability. However, 5-FU has been known to work on only 10~15% of colon cancer patients. Therefore, the study of 5-FU sensitivity study is necessary to increase the survival of colon cancer patients. p53 is one of the factors that effect on drug sensitivity. Main function of p53 has been focused on transcription activity in cell death. Numerous drug related studies show that expression of wild-type p53 increases drug sensitivity in various cancer types through inducing apoptotic signaling pathways. Currently, it has been reported that p53 has both transcriptional and non-transcriptional activities in apoptosis. However, most studies about p53 non-transcriptional activities in apoptosis are mainly focused on p53 induced mitochondrial outer membrane permeabilization, triggering the release of pro-apoptotic factors. The chromatin structure and organization have strongly attracted because of their impacts in cellular phenotypes. Recent studies have been shown that changes in chromatin accessibility affect cell phenotypes for external stimuli. Since p53 plays an important role in drug sensitivity and 5-FU is an external stimulus for cancer cells, we hypothesized that p53 may effect on 5-FU sensitivity through different regulation of chromatin accessible regions between TP53-WT and TP53-KO cells. To determine the effect of p53 on chromatin accessibility modification associated with 5-FU sensitivity, ATAC-seq and RNA-seq were performed under 5-FU treatment on TP53-WT as drug sensitive and TP53-KO as drug resistant HCT116 cells. In this study, we found that 5-FU induces chromatin accessibility in both TP53-WT and TP53-KO cells. Moreover, our results show that 5-FU induced chromatin accessibility increases expression of apoptotic genes in TP53-WT HCT116 cells through p53 non-transcriptional activity in nucleus.
2021-02-10 | GSE157949 | GEO
Project description:aCGH of human melanoma cell lines comparing parental (drug sensitve) vs isogenic drug resistant-derived subline
2014-04-21 | GSE49430 | GEO
Project description:In pancreatic cancer the survival rate is low, as the available treatment options usually only extend survival and seldom produce a cure. Drug resistance and disease reoccurrence is the typical reason for death after cancer diagnosis. 5-Fluorouracil (5-FU) is the main chemostatic used in first line therapy. However the majority of the tumors become resistant to treatment. To investigate acquired 5-FU resistance in pancreatic adenocarcinoma, we established chemoresistant monoclonal cell lines from the Panc03.27 cell line by long-term exposure to 5-FU. In addition to increased expression of markers associated with multidrug resistance, the 5-FU resistant clones showed alterations typical of the process of epithelial-to-mesenchymal transition (EMT), including upregulation of mesenchymal markers and increased invasiveness. Microarray analysis revealed the L1CAM pathway as one of the most upregulated pathways in the chemoresistant clones, which was confirmed on RNA and protein levels. Expression of the adhesion molecule L1CAM is associated with a chemoresistant and migratory phenotype of pancreatic cancer. Using esiRNA targeting L1CAM, or by blocking the extracellular part of L1CAM with monoclonal antibodies, we discovered that the increased invasiveness observed in the chemoresistant cells depends on L1CAM. Using esiRNA targeting β-catenin and/or Slug, we discovered that L1CAM expression depends on Slug rather than β-catenin in the 5-FU resistant cells. We demonstrate a functional link between Slug and the expression level of L1CAM in pancreatic cancer cells having undergone EMT following long-term exposure to 5-FU. Our findings provide further insight into the molecular mechanisms leading to a chemoresistant and migratory phenotype in pancreatic cancer cells and indicate the importance of Slug-induced L1CAM in refractory pancreatic cancer. Examination of expression of 5-Fluorouracil (5-FU) Panc03.27 cell line resistant clone versus expression of 5-FU sensitive clones (NT) in 4 replicates per cell lines
2015-08-11 | E-GEOD-58386 | biostudies-arrayexpress
Project description:Complete growth medium RPMI-1640 which contains 10% FCS, 1% Penicillin-Streptomycin Solution was used for cell culture. Both cell lines were maintained at 37 °C in a humidified atmosphere containing 5% CO2. MTT assay was performed to determine the 5 ‑ FU resistance in both of HCT-8/WT and HCT-8/5-FU cell line.
2017-03-15 | GSE81006 | GEO