Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analyses of autophagy-high and autophagy-low cells from human colon cancer organoids

ABSTRACT: We isolated the human colon cancer cells expressing high leveles and low levels of autophagic activity by introdicing an autophagic flux indicator in organoids and performed RNA-seq analyses.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193936 | GEO | 2023/04/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq analyses of autophagy-high and autophagy-low cells from human colon cancer organoids

Project description:RNA-seq analyses of autophagy-high and autophagy-low cells from human colon cancer organoids

| PRJNA798431 | ENA

RNA-seq of BRAF-V600E_mutated and BRAF-V600E_corrected colon cancer organoids

Project description:We aimed to investigate transcriptional changes in human colon cancer organoids with the BRAF-V600E mutation and in human colon cancer organoids in which the BRAF-V600E mutation was corrected by means of CRISPR genome editing. RNAseq was performed at USEQ at the UMC Utrecht (The Netherlands).

2024-02-21 | E-MTAB-13806 | biostudies-arrayexpress

Bulk RNA-seq of MilliporeSigma SCC300 human iPSC-derived colon organoids compared with undifferentiated human iPSCs and MilliporeSigma SCC321 human patient-derived colon organoids

Project description:Experiment intended to obtain expression profiles of iPSC-derived human colon organoids compared to undifferentiated human iPSCs and a patient-derived colon organoid line

2021-10-25 | E-MTAB-11026 | biostudies-arrayexpress

Loss of smad7 promoted the stromal-myofibroblast transition of endometrium via autophagy

Project description:Background: Abnormal autophagy and TGFβ-SMAD3/7 signaling pathway plays an important role in intrauterine adhesions (IUA); however, the exact underlying mechanisms remain unclear. In this study, we aimed to detect whether SMAD7 effected IUA via regulating autophagy and TGFβ-SMAD3 signaling pathway. Methods: The expression of p-SMAD3 and SMAD7 were detected by Immunohistochemistry. Endometrial fibrosis was detected by masson staining. The expression of protein related to autophagy and fibrosis was detected by western blot. The autophagic flux was monitored via Tandem mRFP-GFP-LC3 fluorescence system. Chip assay was used for SMAD3 binding site analysis. SMAD7 knockout mice were used to investigate the regulation of SMAD7 on intrauterine adhesions and autophagy. Results: we observed that patients with IUA exhibited a lower expression of SMAD7. In endometrial stromal cells, the silencing of SMAD7 inhibited autophagic flux, whereas overexpressed SMAD7 promoted autophagic flux. We also found that SMAD7-mediated autophagic flux regulated stromal-myofibroblast transition. These phenotypes are regulated by the transforming growth factor (TGF)β-SMAD3 signaling pathway. We found that SMAD3 directly binds to the 3ʹ-untranslated region of transcription factor EB (TFEB) and inhibits its transcription. SMAD7 promoted autophagic flux by inhibiting SMAD3, thereby promoting the expression of TFEB. The endometria of SMAD7 knockout mice showed a fibrotic phenotype. Simultaneously, autophagic flux was inhibited. On administering the autophagy activator rapamycin, endometrial fibrosis of SMAD7 gene conditional knockout mice was partially restored. Conclusions: The loss of SMAD7 promotes endometrial fibrosis by inhibited autophagic flux via the TGFβ-SMAD3 pathway. Therefore, this study reveals a potential therapeutic target for IUA.

2024-10-11 | GSE272824 | GEO

Activation of autophagy by starvation and mTOR inhibition in three human cell lines

Project description:The aim of the project was to characterize changes in gene expression that are associated with induced autophagic flux. We engineered HeLa, HEK 293 and SH-SY5Y cell lines to express tandem-fluorecent LC3 (tf-LC3). The ratio of the red and green fluorophores indicated how much of the LC3 is in the acidic interior of lysosomes, which was a proxy measure for autophagic flux. RNA sequencing was performed for the cell lines at baseline and 1h, 15h and 30h after treatments. Additional untreated samples were also sequenced at some but not all time points. Autophagy was induced by amino acid starvation or mTOR inhibition (AZD8055).

2022-08-25 | E-MTAB-12020 | biostudies-arrayexpress

Functional genomics of human colon organoids

Project description:Functional genomics of human colon organoids

| PRJNA589838 | ENA

Illumina Infinium HumanMethylation EPIC beadchip profiling of BRAF-V600E_mutated and BRAF-V600E_corrected colon cancer organoids

Project description:We aimed to investigate genome wide DNA methylation changes in human colon cancer organoids with the BRAF-V600E mutation and in human colon cancer organoids in which the BRAF-V600E mutation was corrected by means of CRISPR genome editing. DNA methylation analysis was performed using the Infinium Methylation EPIC beadchip at the Pathology department of the UMC Utrecht (The Netherlands).

2023-12-20 | E-MTAB-13283 | biostudies-arrayexpress

Cell-matrix adhesion contributes to permeability control in human colon organoids

Project description:Background and aims: Cell-cell adhesion structures (desmosomes and, especially, tight junctions) are known to play important roles in control of transepithelial permeability in the colon. The involvement of cell-matrix interactions in permeability control is less clear. The goals of the present study were to: i) determine if disruption of colon epithelial cell interactions with the extracellular matrix alters permeability control and ii) determine if increasing the elaboration of protein components of cell-matrix adhesion complexes improves permeability control and mitigates the effects of cell-matrix disruption. Results: Treatment of colon organoids with Aquamin® increased the expression of multiple basement membrane and hemidesmosomal proteins as well as keratin 8 and 18. TEER values were higher in the presence of Aquamin® than they were under control conditions. Conclusions: These findings provide evidence that cell-matrix interactions contribute to permeability control in the colon. They suggest that the elaboration of proteins important to cell-matrix interactions can be increased in human colon organoids by exposure to a multi-mineral natural product. Increasing the elaboration of such proteins may help to mitigate the consequences of disrupting cell-matrix interactions on permeability control.

2022-03-14 | PXD026923 | Pride

Illumina Infinium HumanMethylation EPIC beadchip profiling of BRAF-V600E_knock-in and BRAF-wildtype human colon organoids

Project description:We aimed to investigate genome wide DNA methylation changes in human colon organoids in which the BRAF-V600E mutation was introduced by means of CRISPR genome editing and in BRAF-wildtype human colon cancer organoids. DNA methylation analysis was performed using the Infinium Methylation EPIC beadchip at the Pathology department of the UMC Utrecht (The Netherlands).

2023-12-20 | E-MTAB-13290 | biostudies-arrayexpress

Transcriptomic analysis reveals autophagy flux variation within mouse pancreatic cancer organoids

Project description:Murine pancreatic cancer cells (HY15549 cells) established from genetically engineered mouse models (GEMM) of PDAC (p48-Cre+, KrasLSL-G12D/+, Trp53lox/+; KPC mice) were transfected with the GFP-LC3-RFP autophagy flux reporter from Mizushima lab, wherein reduction in the GFP/RFP ratio indicates increase in autophagy flux. Organoids derived from these cells were dissociated into single cells and sorted into autophagy-high (AThi) and autophagy-low (ATlo) populations according to GFP/RFP signal ratio. To validate this reporter, RNA was extracted from these two populations and expression of autophagy/lysosome related genes was examined.

2020-04-16 | GSE145766 | 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