Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE178743 | GEO | 2023/08/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

Project description:Small cell lung cancer (SCLC) is a fatal form of cancer that frequently metastasizes to the brain. Here we investigated the mechanisms allowing SCLC cells to grow in the unique brain microenvironment. We found that neuronal programs upregulated in SCLC cells during tumor progression and upon growth in the brain are critical for SCLC growth in the brain. Mechanistically, the presence of SCLC cells in the brain re-activates astrocytes, which in turn promote the survival of SCLC cells by secreting neuronal pro-survival factors such as SERPINE1. We also identified Reelin, a molecule produced by developing neurons to recruit astrocytes, as a molecule secreted by SCLC cells to recruit astrocytes to the tumor site and promote SCLC growth in the brain. Thus, SCLC cells co-opt mechanisms normally at play between astrocytes and neurons to promote SCLC growth in the brain. Targeting such developmental neuronal programs may help treat brain metastases.

2023-06-22 | GSE179032 | GEO

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

2023-08-09 | GSE178738 | GEO

Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

Project description:Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

| PRJNA741987 | ENA

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human SCLC cell RNA seq]

2023-08-09 | GSE178736 | GEO

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

2023-08-09 | GSE178732 | GEO

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

| PRJNA740266 | ENA

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

| PRJNA740253 | ENA

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human SCLC cell RNA seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human SCLC cell RNA seq]

| PRJNA740251 | ENA

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

| PRJNA740250 | ENA

Vasculogenic mimicry in small cell lung cancer.

Project description:Small cell lung cancer (SCLC) is characterized by prevalent circulating tumour cells (CTCs), early metastasis and poor prognosis. We show that SCLC patients (37/38) have rare CTC subpopulations co-expressing vascular endothelial-cadherin (VE-cadherin) and cytokeratins consistent with vasculogenic mimicry (VM), a process whereby tumour cells form 'endothelial-like' vessels. Single-cell genomic analysis reveals characteristic SCLC genomic changes in both VE-cadherin-positive and -negative CTCs. Higher levels of VM are associated with worse overall survival in 41 limited-stage patients' biopsies (P<0.025). VM vessels are also observed in 9/10 CTC patient-derived explants (CDX), where molecular analysis of fractionated VE-cadherin-positive cells uncovered copy-number alterations and mutated TP53, confirming human tumour origin. VE-cadherin is required for VM in NCI-H446 SCLC xenografts, where VM decreases tumour latency and, despite increased cisplatin intra-tumour delivery, decreases cisplatin efficacy. The functional significance of VM in SCLC suggests VM regulation may provide new targets for therapeutic intervention.

| S-EPMC5105195 | biostudies-literature

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