Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq analysis of HCT-116 colon cancer cells upon lysophosphatidic acid treatment

ABSTRACT: We report the differential gene expression upon the LPA treatment depicting the invasion/metastasisphenomenon and the lipogenesis effect on the colorectal cancer cells HCT-116

ORGANISM(S): Homo sapiens

PROVIDER: GSE104016 | GEO | 2020/09/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA profiling of HCT-116 versus HCT-116 treated with 5-aza-2'-deoxycytidine processing human colon cancer cell lines

Project description:UCRs expression signature of HCT-116 cell lines versus HCT-116 cell line treated with DNA methylation inhibitor 5-aza-2'-deoxycytidine

2010-03-09 | E-MTAB-196 | biostudies-arrayexpress

APC ChIP-seq in HCT-116 colon cancer cell line

Project description:Anti-APC ChIP-seq data were collected from HCT-116 cells and 3,985 genomic sequences were found to be enriched in both independent biological replicates.

2018-05-24 | GSE99262 | GEO

Expression data in HCT-116 colon cancer cell treated with SCD1 inhibitor or in SCD1 knocked out HCT-116 cell

Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.

2017-08-01 | GSE98364 | GEO

RNA-Seq analysis of HCT-116 colon cancer cells upon lysophosphatidic acid treatment

Project description:RNA-Seq analysis of HCT-116 colon cancer cells upon lysophosphatidic acid treatment

| PRJNA407959 | ENA

Differential gene expression of the human colon carcinoma cell line HCT-116 upon Entinostat treatment

Project description:Class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with HDAC inhibitors (such as Entinostat) as well as the specific genetic elimination of HDAC1 and HDAC2 leads to a reduced expression of p53 mRNA levels and a subsequent depletion of mutant p53 protein expression. To investigate other tumor entities we also tested the human colon carcinoma cell line HCT-116, which was treated for 24h with 2ÂµM Entinostat or treated with vehicle control. Total mRNA was isolated and checked for integrity. According to manufacture's recommendation the samples were subjected to microarray analysis using the Affymetrix Human Gene ST 2.0 array chip to discover differentially expressed genes.

2016-06-09 | E-MTAB-4303 | biostudies-arrayexpress

Gene expression data from the HCT-116 colon cancer cell line in the presence or absence of siRNA targeting APC

Project description:Gene expression data were collected by RNA-seq from HCT-116 cells in the presence or absence of siRNA targeting APC and 1,376 transcripts changed in expression following APC silencing were identified relative to scrambled siRNA-transfected and untreated controls.

2018-05-24 | GSE99263 | GEO

Gene expression profile of human colorectal carcinoma HCT 116 cell line treated with imipramine

Project description:The study aim is to evaluate to what extent imipramine treatment of HCT-116 colorectal cell lines does affect fascin1-related or cytoskeleton-associated functions

2020-03-23 | GSE125169 | GEO

Gene alterations by PPAR-gamma agonists in human colorectal adenocarcinoma HCT-116 cells

Project description:We examined the alternation of gene expression by MCC-555, rosiglitazone (RGZ) and 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2) in human colorectal adenocarcinoma HCT-116 cells. Keywords: effects of PPAR-gamma agonists

2008-06-10 | GSE9183 | GEO

Barcode and Whole Exome Sequencing Data of Dabrafenib Resistant 3D-HT-29 and Irinotecan Resistant 3D-HCT-116 Spheroids

Project description:HT-29 and HCT-116 cells were barcoded using the CloneTracker lentiviral barcode library and then dabrafenib and irinotecan resistant derivatives of these cell lines were established, respectively.10 million barcoded HT-29 and HCT-116 cells were seeded equally onto poly-HEMA coated 4xT75 flask (DMSO Control, Replica A, B, C for each drug). After seeding, cells were allowed to form spheroids and barcoded 3D-HT-29 spheroids were treated with dabrafenib at increasing doses starting from IC50/10 dose until IC50/2 dose with monthly doubling of the dosing (16 weeks), and barcoded 3D-HCT-116 cells were treated with irinotecan at increasing doses starting from IC50/4 dose until IC50 dose with weekly doubling of the dosing (4 weeks). Following the end points of treatment for each cell line, DNA was isolated from harvested cell lines and barcode sequencing and whole exome sequencing were carried out.

2023-09-01 | E-MTAB-13216 | biostudies-arrayexpress

Time point studies of bPGN treated HCT-116 cell line

Project description:HCT-116 cell lines were treated with bPGN and treated cells were harvested at time-point 0, 1hour and 24hours. Identification of RNA-interacting pharmacophores could provide new chemical probes and potentially novel RNA-based therapeutics. Herein, using a high-throughput differential scanning fluorimetry assay, we identified small molecule natural products with the capacity to bind the discrete stem-looped structure of pre-miR-21. The most potent compound identified was a prodiginine-type compound, butylcylcoheptyl prodiginine (bPGN), with the ability to inhibit Dicer-mediated processing of pre-miRNA-21 in vitro and in cells. Time dependent RT-qPCR, western blot, and transcriptomic analyses showed modulation of miR-21 expression and its target genes such as PDCD4 and PTEN upon treatment with bPGN, supporting on-target inhibition. Consequently, inhibition of cellular proliferation in HCT-116 colorectal cancer cells was also observed when treated with bPGN. The discovery that bPGN can bind and modulate the expression of regulatory RNAs such as miR-21 helps set the stage for further development of this class of natural product as a molecular probe or therapeutic agents against miRNA-dependent diseases.

2019-04-20 | GSE130101 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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