Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABCA12-mediated ceramide efflux governs breast cancer stem cell function

ABSTRACT: ABCA12-mediated ceramide efflux governs breast cancer stem cell function

PROVIDER: PRJNA909181 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22544106_1.fastq.gz	Fastqsanger.gz
	SRR22544106_2.fastq.gz	Fastqsanger.gz
	SRR22544107_1.fastq.gz	Fastqsanger.gz
	SRR22544107_2.fastq.gz	Fastqsanger.gz
	SRR22544108_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

ABCA12-mediated ceramide efflux governs breast cancer stem cell function

Project description:Cancer stem cells (CSCs) drive tumor growth, metastasis, relapse, and chemoresistance. However, it’s unclear how lipid metabolism, especially sphingolipids metabolism, regulates CSCs and chemoresistance. In this study, we developed spontaneous tumor models expressing a Sox9-GFP transgenic reporter and demonstrated that cancer cells expressing high levels of SOX9 functioned as CSCs in both primary tumors and metastases. Transcriptomics analyses uncovered that SOX9high CSCs upregulate ABCA12 lipid transporter. Functionally, downregulation of ABCA12 impaired cancer stemness and chemoresistance of SOX9high cells. Through lipidomic analysis, we demonstrated that ABCA12 regulates SOX9 expression and cancer stemness by controlling ceramide abundance. Blocking ceramide hydrolysis using acid ceramidase inhibitor D-NMAPPD sensitized tumors to chemotherapy and prevented enrichment of SOX9high CSCs. These data suggest a potential strategy for targeting CSCs and overcoming chemoresistance. We further demonstrated that ceramide inhibits the YAP/TAZ signaling that is required for SOX9 expression in breast CSCs.

2023-11-01 | GSE220178 | GEO

Targeting ABCA12-controlled ceramide homeostasis inhibits breast cancer stem cell function and chemoresistance.

Project description:Cancer stem cells (CSCs) drive tumor growth, metastasis, and chemoresistance. While emerging evidence suggests that CSCs have a unique dependency on lipid metabolism, the functions and regulation of distinct lipid species in CSCs remain poorly understood. Here, we developed a stem cell factor SOX9-based reporter for isolating CSCs in primary tumors and metastases of spontaneous mammary tumor models. Transcriptomic analyses uncover that SOX9high CSCs up-regulate the ABCA12 lipid transporter. ABCA12 down-regulation impairs cancer stemness and chemoresistance. Lipidomic analyses reveal that ABCA12 maintains cancer stemness and chemoresistance by reducing intracellular ceramide abundance, identifying a CSC-associated function of ABCA subfamily transporter. Ceramide suppresses cancer stemness by inhibiting the YAP-SOX9 signaling pathway in CSCs. Increasing ceramide levels in tumors enhances their sensitivity to chemotherapy and prevents the enrichment of SOX9high CSCs. In addition, SOX9high and ABCA12high cancer cells contribute to chemoresistance in human patient-derived xenografts. These findings identify a CSC-suppressing lipid metabolism pathway that can be exploited to inhibit CSCs and overcome chemoresistance.

| S-EPMC10691781 | biostudies-literature

Aging stress and ceramide dependent RNA sequencing expression profiling depends on ceramide synthase 6

Project description:The bioactive sphingolipid ceramide, generated by ceramide synthase, is an adaptive stress effector induced in response to various stress stimuli such as aging. In fact, ceramide synthase (CerS) was first discovered in yeast as a longevity assurance gene (LAG1), as the reduced ceramide generation consequent to LAG1 deletion increased longevity. There are six homologues of mammalian LAG1/ceramide synthases (CerS1-6) that generate ceramides with different fatty acid chain lengths with distinct functions and hydrophobicity. Ceramide can be metabolized by sphingosine kinase 1 or 2 for the generation of pro-survival sphingosine 1-phosphate (S1P), which enhances immune cell egress to the blood stream, activating immune function. Ceramide is known to induce mitophagy and cell death. Here we investigated the role of this sphingolipid pathway in immune function, specifically T cell functions, via high throughput expression profiling.

2021-01-01 | GSE148498 | GEO

RNAseq analysis of 8week old islets from murine Abca12 KO pancreas

Project description:The goal of this study was to identify changes in the transcriptome that occur following Abca12 gene deletion relative to Control islets

2020-02-03 | GSE140378 | GEO

RNAseq analysis of 5week old islets from murine Abca12 KO pancreas

Project description:The goal of this study was to identify changes in the transcriptome that occur following Abca12 gene deletion relative to Control islets

2020-02-03 | GSE140377 | GEO

RNA-Seq analysis of Harlequin Ichrthyosis skin, HI 3D model ABCA12 CRISPR-Cas9 KO cell line

Project description:The biology of Harlequin Ichthyosis (HI), a devastating skin disorder, caused by loss of function mutations in the gene ABCA12, is poorly understood and to date no satisfactory treatment has been developed. We sought to investigate pathomechanisms of Harlequin Ichthyosis which could lead to the identification of safe and effective treatments to improve patients' quality of life. RNA-Seq analysis using normal skin (n=5) and HI patient skin (n=4) were performed to define the effects of loss of ABCA12. Functional annotation clustering analysis showed changes in three common groups: epidermal differentiation, lipid metabolism and inflammation (innate immunity and IFNγ signalling). In HI patient skin, gene expression of STAT1, STAT3 and Interleukin 36 (IL-36) A and G cytokines was significantly upregulated compared to normal skin, whereas IL-37, an inhibitor of innate immunity, was downregulated. RNA-Seq and functional assays were performed to define the effects of loss of ABCA12, using an engineered CRISPR-Cas9 ABCA12 KO 3D model. Functional annotation clustering analysis showed changes in three common groups: epidermal differentiation, lipid metabolism and inflammation.

2020-09-02 | GSE131903 | GEO

Meningeal lymphatic CGRP signaling governs pain via cerebrospinal fluid efflux and neuroinflammation in migraine models

Project description:Meningeal lymphatic CGRP signaling governs pain via cerebrospinal fluid efflux and neuroinflammation in migraine models

| PRJNA1107583 | ENA

Deep mutational scan of a drug efflux pump reveals its structure-function landscape

Project description:Drug efflux is a common resistance mechanism found in bacteria and cancer cells. Although several structures of drug efflux pumps are available, they provide only limited functional information on the phenomenon of drug efflux. Here, we performed deep mutational scanning (DMS) on the bacterial ATP binding cassette (ABC) transporter EfrCD from Enterococcus faecalis to determine the drug efflux activity profile of more than 1400 single variants

2021-11-25 | GSE189399 | GEO

Hair follicles modulate skin barrier function

Project description:We generated KA mutant mice (Krt14-CreERT + ABCA12-flox/flox) and controls (ABCA12-flox/flox) that enabled us to assess the effects of deleting a critical barrier gene, ABCA12, in the skin epidermis following tamoxifen treatment. These studies identified numerous differentially expressed genes (DEGs) upon barrier disruption/ABCA12 deletion, including compensatory upregulation of genes involved with epidermal differentiation and barrier function. Overall, this data-set provides a global view of molecular changes that occur in adult mouse skin following barrier perturbation.

2024-05-20 | GSE254889 | GEO

Neuroblastoma response to C2 ceramide and PARP inhibitor (PJ34)

Project description:Analysis of Neuroblastoma SH-SY5Y cell line treated with C2 ceramide, or combination of C2 ceramide and PJ34. Samples were collected in three time points: 3 hours, 6 hours and 24 hours. Results provide insight into the mechanism of cramide induced cell death and role of poly (ADP-ribose) polymerase in these proces.

2016-11-29 | GSE90587 | 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