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Lineage plasticity in SCLC generates non-neuroendocrine cells primed for vasculogenic mimicry

ABSTRACT: Lineage plasticity in SCLC generates non-neuroendocrine cells primed for vasculogenic mimicry

PROVIDER: PRJEB47606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6753360_1.fastq.gz	Fastqsanger.gz
	ERR6753360_2.fastq.gz	Fastqsanger.gz
	ERR6753361_1.fastq.gz	Fastqsanger.gz
	ERR6753361_2.fastq.gz	Fastqsanger.gz
	ERR6753352_1.fastq.gz	Fastqsanger.gz

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Lineage Plasticity in SCLC Generates Non-Neuroendocrine Cells Primed for Vasculogenic Mimicry.

Project description:IntroductionVasculogenic mimicry (VM), the process of tumor cell transdifferentiation to endow endothelial-like characteristics supporting de novo vessel formation, is associated with poor prognosis in several tumor types, including SCLC. In genetically engineered mouse models (GEMMs) of SCLC, NOTCH, and MYC co-operate to drive a neuroendocrine (NE) to non-NE phenotypic switch, and co-operation between NE and non-NE cells is required for metastasis. Here, we define the phenotype of VM-competent cells and molecular mechanisms underpinning SCLC VM using circulating tumor cell-derived explant (CDX) models and GEMMs.MethodsWe analyzed perfusion within VM vessels and their association with NE and non-NE phenotypes using multiplex immunohistochemistry in CDX, GEMMs, and patient biopsies. We evaluated their three-dimensional structure and defined collagen-integrin interactions.ResultsWe found that VM vessels are present in 23/25 CDX models, 2 GEMMs, and in 20 patient biopsies of SCLC. Perfused VM vessels support tumor growth and only NOTCH-active non-NE cells are VM-competent in vivo and ex vivo, expressing pseudohypoxia, blood vessel development, and extracellular matrix organization signatures. On Matrigel, VM-primed non-NE cells remodel extracellular matrix into hollow tubules in an integrin β1-dependent process.ConclusionsWe identified VM as an exemplar of functional heterogeneity and plasticity in SCLC and these findings take considerable steps toward understanding the molecular events that enable VM. These results support therapeutic co-targeting of both NE and non-NE cells to curtail SCLC progression and to improve the outcomes of patients with SCLC in the future.

| S-EPMC10561473 | biostudies-literature

Lineage plasticity in SCLC generates non-neuroendocrine cells primed for vasculogenic mimicry

Project description:RNA-seq data characterising neuroendocrine (NE) and non-NE cells, cultured on plastic or Matrigel, extracted from small cell lung cancer circulating tumour cell derived explants.

2023-09-17 | E-MTAB-10950 | biostudies-arrayexpress

Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Vasculogenic mimicry has been generally accepted as a new form of tumor vascularization and regarded as an unfavorable prognostic factor in multiple aggressive malignancies. We previously reported the presence of vasculogenic mimicry in osteosarcoma patients. The mechanistic basis for osteosarcoma VM remains unclear. We used microarrays to detail the global programme of gene expression between 143B cells and HOS cells exposed to Matrigel which showed greatly different vasculogenic mimicry formation potential and identified distinct classes of vasculogenic mimicry-realted genes during this process.

2018-09-15 | GSE119975 | GEO

Investigating vasculogenic mimicry in breast cancer

Project description:Investigating vasculogenic mimicry in breast cancer

| PRJNA971220 | ENA

Gene expression profiling of neuroendocrine (NE) and non-neuroendocrine (non-NE) cells derived from ex vivo cultures of small cell lung cancer (SCLC) circulating tumour cell-derived explant (CDX) model

Project description:To determine molecular processes in vasculogenic mimicry (VM) competent human SCLC CDX, we profiled gene expression by RNA sequencing in separated NE (VM deficient) and non-NE (VM competent) cells from four CDX cultured on plastic or on Matrigel.

2023-10-23 | GSE240789 | GEO

Role of EGR1 in vasculogenic mimicry of MDA-MB-231 cells

Project description:Vasculogenic mimicry (VM) is an intriguing phenomenon observed in tumor masses, in which cancer cells organize themselves into capillary-like channels that closely resemble the structure and function of blood vessels. Although VM is believed to contribute to alternative tumor vascularization, the detailed regulatory mechanisms controlling these cellular processes remain poorly understood. Our study aimed to investigate the role of Early Growth Response 1 (EGR1) in regulating VM in aggressive cancer cells, specifically MDA-MB-231 triple-negative breast cancer cells.

2023-08-15 | GSE240489 | GEO

Erianin abrogates vasculogenic mimicry through targeting m5C methylase NSUN2

Project description:Erianin abrogates vasculogenic mimicry through targeting m5C methylase NSUN2

| PRJNA1181520 | ENA

Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

| PRJNA490884 | ENA

Role of EGR1 in vasculogenic mimicry of MDA-MB-231 cells

Project description:Role of EGR1 in vasculogenic mimicry of MDA-MB-231 cells

| PRJNA1003903 | ENA

Erianin abrogates vasculogenic mimicry through targeting m5C methylase NSUN2

Project description:Purpose: The precise temporal and spatial regulation of N5-methylcytosine (m5C) RNA modification plays essential roles in RNA metabolism. Targeting m5C regulation in cancer cells may be a potential strategy for cancer therapy. Erianin is a natural product isolated from Dendrobium chrysotoxum Lindl. Howbeit, the in‐depth understanding of interaction between erianin and m5C modification remains indistinct. Methods: Natural product library screening was used to explore the effects of natural product monomers on uveal melanoma (UM) cells. Intraocular xenografts model was established to examine the effect of erianin. Immunoprecipitation mass spectrometry (IP-MS) and molecular docking analyses were performed to identify NSUN2 as the target of erianin. m5C-meRIP-seq and m5C-meRIP-qPCR analyses were performed to identify the functional target of NSUN2. Tube formation assay and CD31-PAS double staining were used to detect vasculogenic mimicry (VM) in UM. Results: Herein, we report the discovery of erianin as an effective inhibitor of uveal melanoma. Mechanistically, the targeted inhibition of NSUN2 function by erianin results in a decrease in the m5C modification and expression levels of CHAC1 in UM, thereby curtailing the formation of VM. Conclusions: Collectively, our data suggested that erianin significantly inhibited UM progression in vitro and in vivo. Our study unveils a novel therapeutic strategy for combating UM.

2024-12-10 | GSE280936 | GEO

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