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Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

ABSTRACT: Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Single cell RNA-Seq)

PROVIDER: PRJNA647895 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12298113.fastq.gz	Fastqsanger.gz
	SRR12298114.fastq.gz	Fastqsanger.gz
	SRR12298115.fastq.gz	Fastqsanger.gz
	SRR12298116.fastq.gz	Fastqsanger.gz

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Phenotypic plasticity underlies local invasion and distant metastasis in ovarian cancer

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Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer (Bulk RNA-Seq)

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Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer.

Project description:Phenotypic plasticity represents the most relevant hallmark of the carcinoma cell as it bestows it with the capacity of transiently altering its morphological and functional features while en route to the metastatic site. However, the study of phenotypic plasticity is hindered by the rarity of these events within primary lesions and by the lack of experimental models. Here, we identified a subpopulation of phenotypic plastic colon cancer cells: EpCAMlo cells are motile, invasive, chemo-resistant, and highly metastatic. EpCAMlo bulk and single-cell RNAseq analysis indicated (1) enhanced Wnt/β-catenin signaling, (2) a broad spectrum of degrees of epithelial to mesenchymal transition (EMT) activation including hybrid E/M states (partial EMT) with highly plastic features, and (3) high correlation with the CMS4 subtype, accounting for colon cancer cases with poor prognosis and a pronounced stromal component. Of note, a signature of genes specifically expressed in EpCAMlo cancer cells is highly predictive of overall survival in tumors other than CMS4, thus highlighting the relevance of quasi-mesenchymal tumor cells across the spectrum of colon cancers. Enhanced Wnt and the downstream EMT activation represent key events in eliciting phenotypic plasticity along the invasive front of primary colon carcinomas. Distinct sets of epithelial and mesenchymal genes define transcriptional trajectories through which state transitions arise. pEMT cells, often earmarked by the extracellular matrix glycoprotein SPARC together with nuclear ZEB1 and β-catenin along the invasive front of primary colon carcinomas, are predicted to represent the origin of these (de)differentiation routes through biologically distinct cellular states and to underlie the phenotypic plasticity of colon cancer cells.

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A blueprint for local and distal glioblastoma invasion programs

Project description:Glioblastoma (GBM) invasion into brain parenchyma presents significant challenges for treatment but remains poorly understood. In this study, we combined single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and multiplexed imaging of orthotopic xenograft models to investigate GBM invasion. We first screened 20 patient-derived gliomasphere models for their distal (i.e., extending to the contralateral hemisphere) and local invasive potential in mice. We found that models with distal invasion potential are enriched with oligodendrocyte progenitor-like (OPC-like) cells, while models with only local invasion potential are enriched with mesenchymal-like (MES-like) cells. These patterns reflect predominantly peri-axonal vs peri-vascular invasion routes, respectively. Next, we analyzed the transcriptomes of invading cells within models (compared to tumor core) and identified novel programs associated with distal and local invasion. Thus, we decouple transcriptional features associated with invasion potential from those associated with the process of invasion. We validated our findings by spatial transcriptomics and multiplexed imaging, further describing the spatial niche of invasive cells. Taken together, our results provide a blueprint for the invasive potential of GBM cell states and of the programs associated with invasion across different scales.

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Project description:Recurrent/metastatic head and neck squamous cell carcinoma (R/M-HNSCC) is a severe, frequently lethal condition. Targeted therapy includes epidermal growth factor receptor (EGFR) blockade, but overall response rates are low and predictive biomarkers amiss. Deepened understanding of molecular networks governing EGFR-driven progression are required to explore predictive markers and therapeutic targets. We have mapped EGFR-mediated local invasion in a 3D-model using photoconvertible cell-tracers and uncovered invasion-associated, differentially expressed genes (DEGs) correlated with EGFR/MAPK activity and epithelial-to-mesenchymal transition (EMT) in primary malignant cells. A gene regulatory network (GRN) of local invasion was defined, composed of the central hubs inhibin subunit beta alpha (INHBA) and SLUG, and druggable effectors integrin subunit beta 4 (ITGβ4), its ligand laminin 5 (LAMB3/LAMC2), sphingosine kinase 1 (SPHK1), and EGFR ligand amphiregulin (AREG). Blockade of INHBA repressed local invasion, which was rescued by Activin A, Laminin 5, and sphingosine-1-phosphate, proving functional interconnection of the GRN. Functional DEGs (fDEGs) and, most prominently, central hub IHNBA, were associated with tumor buds in TCGA-HNSCC. Newly defined EGFR-activity subtypes, primarily dictated by AREG and epiregulin (EREG), show enhanced fDEGs expression, EMT correlation, and prognostic value. Cell-communication revealed strong interactions of AREG/EREG-governed EGFR-activities with non-malignant cells, potentially impacting on tumor progression. High expression of fDEGs enriched in EGFR-activities (INHBA, ITGA3, ITGΒ4, LAMA3, LAMC2, MT2A, EREG) was associated with response to Cetuximab in PDX models and R/M-HNSCC patients. Thus, we describe a novel GRN of EGFR-mediated local invasion and define druggable effectors with predictive potential regarding the response to Cetuximab.

2025-03-26 | GSE273463 | GEO

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