Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mitochondrial fusion drives oxidative metabolism to immortalize neural stem cells during tumorigenesis

ABSTRACT: Mitochondrial fusion drives oxidative metabolism to immortalize neural stem cells during tumorigenesis

PROVIDER: PRJNA645416 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12194200.fastq.gz	Fastqsanger.gz
	SRR12194300.fastq.gz	Fastqsanger.gz
	SRR12194400.fastq.gz	Fastqsanger.gz
	SRR12194500.fastq.gz	Fastqsanger.gz
	SRR12194201.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 384

Similar Datasets

Mitochondrial fusion drives oxidative metabolism to immortalize neural stem cells during tumorigenesis

Project description:Metabolic reprogramming is a key feature of many cancers, but how and when it contributes to tumorigenesis remains unclear. Here, we demonstrate that metabolic reprogramming induced by mitochondrial fusion can be rate-limiting for immortalization of tumor initiating cells (TICs) and trigger their irreversible dedication to tumorigenesis. Using single-cell transcriptomics, we find that Drosophila brain tumors contain a rapidly dividing stem cell population defined by upregulation of oxidative phosphorylation (OxPhos). We combine targeted metabolomics and in-vivo genetic screening to demonstrate that OxPhos is required for tumor cell immortalization but is dispensable in the neural stem cells (NSCs) giving rise to the tumors. Employing an in-vivo NADH/NAD+ sensor, we show that NSCs increase OxPhos precisely during immortalization. Blocking OxPhos or mitochondrial fusion stalls the TICs in quiescence and prevents tumorigenesis through impaired NAD+ regeneration. Our work establishes a unique connection between cellular metabolism and the immortalization of tumor initiating cells.

2020-07-13 | GSE154203 | GEO

Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

Project description:Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

| PRJNA1006401 | ENA

Notch3 drives meningioma tumorigenesis and resistance to radiotherapy

Project description:Notch3 drives meningioma tumorigenesis and resistance to radiotherapy

| PRJNA988146 | ENA

Phase separation of YAP fusion proteins drives supratentorial ependymoma

Project description:Phase separation of YAP fusion proteins drives supratentorial ependymoma

| PRJNA854642 | ENA

Phase separation of YAP fusion proteins drives supratentorial ependymoma I

Project description:HIPPO-YAP/TAZ signaling has been implicated in supratentorial ependymoma formation from neural progenitor cells (NPC) in the brain, however, the underlying mechanisms to trigger the neural progenitor cell transformation remains elusive. Here, we uncover that patient-derived tumorigenic YAP-fusion proteins (YAP-MAMLD1 and C11ORF95-YAP) promote ependymoma tumorigenesis through forming liquid-liquid phase-separated condensates. Intrinsically disordered regions (IDR) in the fusion proteins promote oligomerization of YAP-transcriptional co-activators and self-assembly of nuclear puncta-like membrane-less organelles. Phase separation of YAP-fusion proteins further facilitates the compartmentalization of transcriptional coactivators, BRD4 and MED1, resulting in pervasive enhancer landscape changes and exclusion of transcriptional repressors such as PRC2 complexes. YAP-fusion proteins-induced nuclear puncta recruit RNA polymerase II to promote transcriptional bursting of multiple oncogenic pathways. Moreover, we show that IDR-mediated phase separation is necessary for YAP-fusion protein-induced tumor formation. Distinct YAP fusion-proteins identified in other human tumors also encompass IDR features. Together, our data suggest that IDR-mediated phase separation is an integral component of YAP-fusion protein-induced tumorigenesis and might serve as a therapeutic target in supratentorial ependymoma.

2022-10-27 | GSE181867 | GEO

Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

Project description:Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

| PRJNA407757 | ENA

Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

Project description:Fusion of the N-terminus of the mixed-lineage-leukemia (MLL) gene with various partner genes drives acute lymphoblastic leukemia (ALL). Despite the fusion proteins sharing some common attributes, transcriptome heterogeneity of MLL-fusion ALL is observed and the underlying mechanism and biological consequences are unknown. We compared the genome-wide occupancy of MLL-Af4 and MLL-AF9 in human ALL cells expressing FLAG-tagged fusion proteins. Although both oncoproteins retain the same MLL N-terminal domains that mediate chromatin binding, the two fusion proteins displayed largely non-overlapping binding profiles, with MLL-AF9 showing preferential binding at repetitive elements. The binding specificity of each fusion protein was associated with differential global gene activation distinguishing the two ALLs. A subset of prednisolone response genes were among the differentially regulated targets, and the resistance related genes were specifically upregulated in MLL-Af4/AF4 cells. These studies provide evidence that distinct chromatin occupancy of different MLL-fusion proteins is one driving force for transcriptome heterogeneity of MLL-fusion ALL, which could potentially result in the disparate therapeutic outcome of the disease.

2018-04-30 | GSE103947 | GEO

Oncogenic ALKF1174L drives tumorigenesis in cutaneous squamous cell carcinoma

Project description:Oncogenic ALKF1174L drives tumorigenesis in cutaneous squamous cell carcinoma

| PRJNA615866 | ENA

Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma [RNA-Seq]

Project description:Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma [RNA-Seq]

| PRJNA1006404 | ENA

FOXO3 Deficiency in Neutrophils Drives Colonic Inflammation and Tumorigenesis

Project description:FOXO3 Deficiency in Neutrophils Drives Colonic Inflammation and Tumorigenesis

| PRJNA979263 | ENA