Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next-generation sequencing analysis of transcriptom in gemcitabine resistant pancreatic cancer cells

ABSTRACT: Next-generation sequencing was applied to compare the transcriptom of 1) SW1990 human pancreatic cancer cell lines and its gemcitabine-resistant derivative established with long-term exposure in medium containing 100 nM gemcitabine; 2) TRA-1-81+ cells and TRA-1-81- cells isolated from SW1990 human pancreatic cancer cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE79953 | GEO | 2017/03/31

SECONDARY ACCESSION(S): PRJNA317483

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Exploring Transcriptional alterations in the Development of Gemcitabine Resistance [SW1990R_vs_SW1990_RNAseq]

Project description:To investigate the transcriptional alterations that occur during the development of gemcitabine resistance in pancreatic cancer cells, we established gemcitabine-resistant SW1990 cells, referred to as SW1990R. We then employed RNA-seq to explore the transcriptome changes between the gemcitabine-resistant cells and their parental counterparts.

2024-09-23 | GSE247165 | GEO

Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [SW1990R_vs_SW1990_RRBS]

Project description:To elucidate the DNA methylation alterations during the development of gemcitabine resistance in pancreatic cancer cells, we utilized both the parental SW1990 cells and their gemcitabine-resistant derivatives, SW1990R cells, to examine DNA methylation patterns. We employed reduced representation bisulfite sequencing (RRBS) assays to uncover the specific CpG methylation profiles.

2024-09-23 | GSE247167 | GEO

Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [SW1990R_vs_SW1990_ATACseq]

Project description:To elucidate the epigenetic events, particularly the dynamic alterations in chromatin accessibility during the development of gemcitabine resistance in pancreatic cancer cells, both the parental SW1990 cells and the gemcitabine-resistant counterparts, SW1990R cells, were employed for mapping of the chromatin accessibility landscape. The ATAC-seq technology was used for precise detection of chromatin accessibility.

2024-09-23 | GSE251994 | GEO

Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [SW1990R_vs_SW1990_CUTTAG]

Project description:To elucidate the epigenetic events, particularly the dynamic alterations in chromatin states during the development of gemcitabine resistance in pancreatic cancer cells, both the parental SW1990 cells and the gemcitabine-resistant counterparts, SW1990R cells, were employed for mapping of the histone modification landscape. The CUT&Tag-seq technology was used for precise detection of histone marks, including H3K4me1 (associated with enhancers), H3K27ac (related to active enhancers and promoters), H3K4me3 (linked to PolII-bound and CpG-rich promoters), H3K9me3 (associated with heterochromatin regions), and H3K27me3 (indicative of Polycomb inhibition).

2024-09-23 | GSE247164 | GEO

Nrf2 depletion sensitizes pancreatic cancer cells to gemcitabine via aldehyde dehydrogenase 3a1 repression.

Project description:The central regulator of oxidative stress responses, Nrf2, is attracting great interest as a therapeutic target in various cancers. Explorations of novel Nrf2 inhibitors have been reported, which suggest future clinical applications. Halofuginone, the derivative of natural plant alkaloid, has been reported to deplete Nrf2 rapidly in cancer cells with Nrf2 activation. In the current study, we identified that halofuginone sensitizes pancreatic cancer cells to gemcitabine, both in vitro and in vivo settings. We identified downregulation of Aldh3a1 in mouse pancreatic cancer cell lines after halofuginone treatment. The Nrf2 inducer diethyl maleate treatment upregulated Aldh3a1, and Nrf2 deleted pancreatic cancer cell lines failed to show induction. Knockdown of Aldh3a1 also sensitized cancer cells to gemcitabine, suggesting contribution of Aldh3a1 to gemcitabine resistance as a downstream target of Nrf2. Current study confirmed the therapeutic benefits of halofuginone in pancreatic cancer.

2021-12-21 | GSE172046 | GEO

MIA PaCa-2 cells treated with Gemcitabine

Project description:Pancreatic cancer cells (MIA PaCa-2) were treated with Gemcitabine and overall protein changes were studied

2022-09-15 | PXD030861 | Pride

mRNA-seq of gemcitabine resistant pancreatic cancer cell line subclones derived from BxPC3

Project description:We generated gemcitabine resistant subclones from the human pancreatic cancer cell line BxPC3 using chronic low dose exposure to gemcitabine. Three gemcitabine resistant subclones (BxGR-80C, BxGR-120C and BxGR-360C) were sequenced in addition to BxPC3 cells.

2021-12-21 | E-MTAB-11186 | biostudies-arrayexpress

Expression data from gemcitabine treated pancreatic CAFs

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naÃ¯ve CAFs (N-CAFs) and R-CAFs were compared by array analysis. Immortalized human pancreatic CAFs were grown for 30 days in either control media or media containing 100nM gemcitabine. RNA was then isolated and hybidized on U133 Plus 2.0 Affymetrix arrays.

2016-03-09 | E-GEOD-78982 | biostudies-arrayexpress

Exploring Transcriptional alterations in the Development of Gemcitabine Resistance [AsPC1R_vs_AsPC1_RNAseq]

Project description:To investigate the transcriptional alterations that occur during the development of gemcitabine resistance in pancreatic cancer cells, we established gemcitabine-resistant AsPC1 cells, referred to as AsPC1R. We then employed RNA-seq to explore the transcriptome changes between the gemcitabine-resistant cells and their parental counterparts.

2024-09-23 | GSE247163 | GEO

In vivo response of EpCAM+ pancreatic cancer cells to gemcitabine plus anti-LIF neutralizing antibody treatment

Project description:The goal of this study is to investigate the molecular mechanisms of LIF action on pancreatic cancer cells in the classical pancreatic ductal adenocarcinoma mouse model KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice EpCAM+ pancreatic cancer cells were isolated from pancreatic tumors developped in KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice treated with either gemcitabine plus control IgG or gemcitabine plus anti-LIF antibody by FACS

2018-12-21 | GSE99187 | 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