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Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma (Digital Spatial Profiling)

ABSTRACT: Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma (Digital Spatial Profiling)

PROVIDER: PRJNA866548 | ENA |

REPOSITORIES: ENA

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Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma (Digital Spatial Profiling)

Project description:To progress, tumors need to invade the surrounding tissues. However, the heterogeneity of cell types at the tumor-stroma interface and the complexity of their potential interactions hampered mechanistic insights for efficient therapeutic targeting. Here, combining single-cell and spatial transcriptomics on human basal cell carcinomas (BCCs), we define the cellular contributors of the invasive front. In the invasive niche, tumor cells harbor a collective migration phenotype, supported by the expression of cell-cell junction complexes. In physical proximity, we identify cancer-associated fibroblasts (CAFs) with extracellular matrix-remodeling features, as required to support collective migration. Moreover, while tumor cells specifically express Activin A, we find Activin A-induced gene signature enrichment in adjacent CAFs subpopulations, further supporting their biological crosstalk. Altogether, our data identify the subpopulations and their transcriptional reprogramming contributing to the spatial organization of the BCC invasive niche. They also bring the proof-of-concept for integrated spatial and single-cell multi-omics to decipher cancer-specific invasive properties and develop therapeutic targeting.

2022-08-06 | GSE210648 | GEO

Integrated multi-omics reveals the cellular and molecular interactions governing the invasive niche in skin cancer

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Integrated multi-omics reveals cellular and molecular interactions governing the invasive niche of basal cell carcinoma.

Project description:Tumors invade the surrounding tissues to progress, but the heterogeneity of cell types at the tumor-stroma interface and the complexity of their potential interactions hampered mechanistic insight required for efficient therapeutic targeting. Here, combining single-cell and spatial transcriptomics on human basal cell carcinomas, we define the cellular contributors of tumor progression. In the invasive niche, tumor cells exhibit a collective migration phenotype, characterized by the expression of cell-cell junction complexes. In physical proximity, we identify cancer-associated fibroblasts with extracellular matrix-remodeling features. Tumor cells strongly express the cytokine Activin A, and increased Activin A-induced gene signature is found in adjacent cancer-associated fibroblast subpopulations. Altogether, our data identify the cell populations and their transcriptional reprogramming contributing to the spatial organization of the basal cell carcinoma invasive niche. They also demonstrate the power of integrated spatial and single-cell multi-omics to decipher cancer-specific invasive properties and develop targeted therapies.

| S-EPMC9391376 | biostudies-literature

Integrated multi-omics reveals the cellular and molecular interactions governing the invasive niche in skin cancer

Project description:Integrated multi-omics reveals the cellular and molecular interactions governing the invasive niche in skin cancer

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Transcription profiling of Aspergillus fumigatus isolates following laboratory culture or initiation of infection in the neutropenic murine lung to understand how metabolic and nutritional factors governing adaptation to the host niche contribute to virulence

Project description:To understand how metabolic and nutritional factors governing adaptation to the host niche contribute to the virulence of Aspergillus fumigatus we compared transcriptomes of developmentally matched A.fumigatus isolates following laboratory culture or initiation of infection in the neutropenic murine lung.

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A correctable immune niche for basal-epithelial stem-cell reprogramming and post-viral lung diseases

Project description:Epithelial barriers are programmed for defense and repair but are also frequently the site of long-term remodeling disease. In general, this paradigm features activation of epithelial stem cells that coordinate organ development but persist into adult life to regenerate damaged tissues. Here we identify a Wfdc21-dependent monocyte-derived dendritic cell (moDC) population that functions as an early sentinel niche for basal-epithelial stem cells (basal-ESC) growth and feed-forward inflammation in mouse models of epithelial injury due to respiratory viral infections. This niche function depends on Gpnmb-CD44 signaling so that transient but properly timed antibody blockade of ligand or receptor provides long-lasting disease correction in these injuries. These same control points are found for mouse and human basal-ESC-derived organoids, and the corresponding biomarkers track with comparable lung diseases in humans. Together, the findings identify a mechanism to explain and modify basal-ESC reprogramming in what is otherwise a stereotyped, primordial response to epithelial injury.

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Basal-to-inflammatory transition enhances basal cell carcinoma (BCC) therapy resistance via crosstalk with a pro-inflammatory stromal niche

Project description:Basal-to-inflammatory transition enhances basal cell carcinoma (BCC) therapy resistance via crosstalk with a pro-inflammatory stromal niche

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Basal-to-inflammatory transition contributes to basal cell carcinoma therapy resistance via crosstalk with a pro-inflammatory stromal niche

Project description:Basal-to-inflammatory transition contributes to basal cell carcinoma therapy resistance via crosstalk with a pro-inflammatory stromal niche

| PRJNA1024039 | ENA

Basal-to-inflammatory transition contributes to basal cell carcinoma therapy resistance via crosstalk with a pro-inflammatory stromal niche

Project description:Basal-to-inflammatory transition contributes to basal cell carcinoma therapy resistance via crosstalk with a pro-inflammatory stromal niche

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Quiescent horizontal basal stem cells act as a niche for olfactory neurogenesis in a 3D organoid model

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