Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Melanoma cell acquired resistance to vinca-alkaloids

ABSTRACT: Malignant melanoma (MM) remains a therapeutic challenge on account of extreme primary resistance to apoptosis and fated acquired chemoresistance. In the current context of molecular classification of MM, the understanding of molecular mechanisms giving rise to these resistances should drive therapeutic choice trough personalized medicine. In order to study mechanisms of MM acquire resistance to VAs, we previously established three VA-resistant cell lines, CAL1R-VCR, CAL1R-VDS, and CAL1R-VRB, by long time exposure of the CAL1-wt MM cell line to IC50 (4nM) of VCR, VDS and VRB respectively. CAL1R-VAs cell lines consisted of polyclonal populations to respect biological diversity of tumour. Then, we searched for determine the resistance process impact on MM cells. We thus performed genome-wide analyses based on comparison of global transcriptomic profile of CAL1R-VAs cells to CAL1-wt. In this way, RNA extracted from each cell line was hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. After hybridization, microarray data were processed with Robust Multi-array Average (RMA) algorithm. We then performed bioinformatic analyses of microarray data and in vitro investigations in the aim to identify genes and pathways that might predict drug resistance. Melanoma model: CAL1 cell line. Treatments: vinorelbine (VRB), vincristine (VCR), vindesine (VDS). Etablishment of 3 resistant cell lines by long time exposure to vinka-alkaloids (4nM, 6-12 months): CAL1R-VRB, CAL1R-VCR, CAL1R-VDS. RNA extracted from a pooled population of each cell line were hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. Then, microarray data were processed with Robust Multi-array Average (RMA) algorithm.

ORGANISM(S): Homo sapiens

SUBMITTER: Laure-Anais Vincent

PROVIDER: E-GEOD-61007 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Melanoma cell acquired resistance to vinca-alkaloids

Project description:Malignant melanoma (MM) remains a therapeutic challenge on account of extreme primary resistance to apoptosis and fated acquired chemoresistance. In the current context of molecular classification of MM, the understanding of molecular mechanisms giving rise to these resistances should drive therapeutic choice trough personalized medicine. In order to study mechanisms of MM acquire resistance to VAs, we previously established three VA-resistant cell lines, CAL1R-VCR, CAL1R-VDS, and CAL1R-VRB, by long time exposure of the CAL1-wt MM cell line to IC50 (4nM) of VCR, VDS and VRB respectively. CAL1R-VAs cell lines consisted of polyclonal populations to respect biological diversity of tumour. Then, we searched for determine the resistance process impact on MM cells. We thus performed genome-wide analyses based on comparison of global transcriptomic profile of CAL1R-VAs cells to CAL1-wt. In this way, RNA extracted from each cell line was hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. After hybridization, microarray data were processed with Robust Multi-array Average (RMA) algorithm. We then performed bioinformatic analyses of microarray data and in vitro investigations in the aim to identify genes and pathways that might predict drug resistance.

2014-09-03 | GSE61007 | GEO

Exploring the Mechanism of Resistance to vincristine in Breast Cancer Cells through Transcriptome Sequencing Technology

Project description:Breast cancer has replaced lung cancer as the leading cancer globally, but various chemotherapy drugs for breast cancer are prone to generate resistance, especially in patients with distant metastases who are susceptible to multiple chemotherapy drug resistance, these always leading to treatment failure. vincristine (VCR) is an alkaloid extracted from Catharanthus roseus and is often used in combination with other chemotherapy drugs to treat various types of cancer, including breast cancer. Recently, we conducted research on the development of resistance to VCR using transcriptome sequencing technology. Firstly, we used the gradient increase of VCR concentration to produce a VCR-resistant breast cancer cell line. Mechanistically, we further extracted RNA from the VCR-resistant breast cancer cell line and sequenced the transcriptome. Further analysis showed changes in various gene expression levels in the VCR-resistant breast cancer cell line. Meanwhile, the analysis of splicing events also indicated that variable splicing events change in the VCR-resistant breast cancer cell line. Further validation showed that multiple gene expression levels, including 1L1B, were altered in the VCR-resistant breast cancer cell line, and these gene expression changes were related to VCR resistance. Our results provide a theoretical basis for exploring the mechanism of VCR resistance clinically.

2023-09-12 | GSE241356 | GEO

Expression profiling of long non-coding and coding gene expression of gastric cancer cell lines

Project description:The high throghput lncRNA and mRNA microarray data showed a total of 27,883 lncRNAs and 19,644 mRNAs expressed in gastric cancer cell line, SGC7901 and two multidrug-resistance sublines, SGC7901/ADR and SGC7901/VCR

2015-05-29 | GSE69342 | GEO

Genome-wide expression analysis of a human pDC cell line

Project description:Analysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4) Keywords: Genome-wide expression analysis

2008-10-02 | GSE12507 | GEO

Transcription profiling of human pDC cell line

Project description:Analysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4) Experiment Overall Design: Duplicates of both CAL1 and MOLT4 cells used

2008-10-26 | E-GEOD-12507 | biostudies-arrayexpress

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

Project description:Combined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh. We used microarrays to detail the global changes in gene expression of Reh cells upon enforced expression of miR-125 per se compared with combination of overexpression of miR-125b, miR-100 and/or miR-99a MiR-99a and/or miR-100 were transiently overexpressed in stable miR-125b-expressing and stable scrambled miR-control-expressing Reh cells. Cellular resistance to VCR was determined by MTT assay after incubating the cells with 9 ng/mL VCR for 3 days. Changes in the gene expression pattern of Reh cells induced by miRNAs overexpression were measured using Affymetrix Arrays.

2013-06-27 | E-GEOD-46362 | biostudies-arrayexpress

Changes in Gene Expression Profile in two Multidrug Resistant Cell Lines derived from a same Drug Sensitive Cell line

Project description:Resistance to chemotherapy is one of the most relevant aspects of treatment failure in cancer. Cell lines are used as models to study resistance. We analyze the transcriptional profile of two multidrug resistant (MDR) cell lines (Lucena 1 and FEPS) derived from the same drug-sensitive cell K562. Microarray data identified 130 differentially expressed genes (DEG) between K562 vs Lucena, 1,932 between K562 vs FEPS, and 1,211 between Lucena 1 versus FEPS. The NOTCH pathway was affected in FEPS with overexpression of NOTCH2 and HEY1. The highly overexpressed gene in MDR cell was ABCB1, and both presented the ABCB1 promoter unmethylated. Gene expression profiles were obtained with the GeneChip® Human Genome U133 Plus 2.0 Array (Affymetrix, Singapore) according to the manufacturer´s instructions; all hybridization experiments were carried out in duplicate. The following samples were analyzed: human K562 cell line RNA from cells grown without drugs; human Lucena 1 cell line RNA from cells grown in medium with vincristine (Lucena 1+VCR); Lucena 1 cell line RNA from cells grown in medium without drugs (Lucena 1-VCR); human FEPS cell line RNA from cells grown in medium with daunorubicin (FEPS +DNR), and FEPS cell line RNA from cells grown in medium without drugs (FEPS -DNR).Comparisons of microarray expression data were carried out between K562 vs Lucena 1 grown in medium without vincristine; K562 vs FEPS grown in medium without daunorubicin; Lucena 1 grown in medium without vincristine vs FEPS grown in medium without daunorubicin. Additionally, we compared expression profiles of each multidrug resistant cell line (Lucena 1 and FEPS) grown in different conditions: Lucena 1 grown in medium without vincristine vs Lucena 1 grown in medium with vincristine, and FEPS grown in medium without daunorubicin vs FEPS grown in medium with daunorubicin.

2015-01-01 | E-GEOD-57470 | biostudies-arrayexpress

Vincristine resistance reshapes sphingolipid composition and promotes mitochondrial complex I deficiency in acute myelogenous leukemia

Project description:Modifications in sphingolipid (SL) metabolism and mitochondrial bioenergetics are key factors implicated in cancer cell response to chemotherapy, including chemotherapy resistance. Vinca alkaloids such as vincristine (VCR), widely used in cancer treatment, are no exception, as their beneficial actions are often supplanted by resistance. In the present work we utilized HL-60 human leukemia cells and a VCR-resistant counterpart, HL-60/VCR cells, to determine whether VCR resistance affected alterations in SL composition and mitochondrial bioenergetics supportive of a neoplastic phenotype. HL-60/VCR cells, as opposed to wild-type cells, showed striking increases in sphingosine 1-phosphate (S1P) supportive of mitogenicity and disease dissemination. VCR resistance was also characterized by increases in ceramides as well as glucosylceramides (GC), and decreases in levels of sphingomyelin. Immunoblot analysis revealed upregulated expression of sphingosine kinase (SPHK1), which catalyzes formation of S1P, glucosylceramide synthase, which catalyzes formation of GC, and acid ceramidase, responsible for ceramide hydrolysis. With respect to mitochondria, despite increased basal respiration in VCR cells, direct interrogation of the VCR mitochondrial network revealed intrinsic respiratory complex insufficiency, largely localized to complex I (CI). Importantly, intrinsic CI limitations were completely masked using traditional intact cell respirometry, thus highlighting the critical importance of comprehensive bioenergetic phenotyping to elucidate metabolic remodeling in drug resistance. Together, these data underscore the intimate connection between cellular sphingolipids and mitochondrial metabolism and suggest that pharmacological intervention across both pathways may represent a novel treatment strategy against VCR resistance.

2022-04-21 | PXD025645 | JPOST Repository

Expression data from Drosophila S2 cells

Project description:An Affimetrix GeneChip Drosophila genome 2.0 array was used to study the effect of protocatechuic aldehyde on gene expression. The addition of 0.1 mM protocatechuic aldehyde to Drosophila S2 cells significantly affected the expression of 52 genes, with 29 being up-regulated and 23 being down-regulated.

2012-05-03 | GSE37701 | GEO

Expression data from human subcutaneous adipocytes

Project description:An Affimetrix GeneChip Human Genome U133 Plus 2.0 Array was used to study the effect of oleoylethnolamide on gene expression. The addition of 0.01 mM oleoylethanolamide (OEA) to human subcutaneous adipocytes significantly affected the expression of 1013 genes, with 556 being up-regulated and 457 being down-regulated.

2014-11-04 | GSE55539 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data