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Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts

ABSTRACT: Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts

PROVIDER: PRJNA962180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24319300_1.fastq.gz	Fastqsanger.gz
	SRR24319300_2.fastq.gz	Fastqsanger.gz
	SRR24319301_1.fastq.gz	Fastqsanger.gz
	SRR24319301_2.fastq.gz	Fastqsanger.gz
	SRR24319302_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts

Project description:In this study, we investigated extracellular vesicle (EVs)-mediated intercellular communication between cutaneous squamous cell carcinoma (cSCC) cells and surrounding stroma cells in tumor microenvironment (TME). Interfering with capacity of cSCC cells to secrete EVs resulted by depletion of RAB27A inhibits cSCC tumor growth in vivo.Transcriptome analysis of tumor xenografts by RNA-seq enabling the identification of both human and mouse transcripts revealed wide-spread changes both in mouse and human cells. Impaired EV-production prominently altered the phenotype of stomal cells, in particular genes related to extracellular matrix (ECM)-formation and epithelial-mesenchymal transition (EMT). This was paralleled by transcriptomic changes in the human tumor cells showing signs of activated p53 pathway and cell apoptosis.

2023-07-27 | GSE230706 | GEO

Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts.

Project description:Cutaneous squamous cell carcinoma (cSCC) is a fast-increasing cancer with metastatic potential. Extracellular vesicles (EVs) are small membrane-bound vesicles that play important roles in intercellular communication, particularly in the tumor microenvironment (TME). Here we report that cSCC cells secrete an increased number of EVs relative to normal human epidermal keratinocytes (NHEKs) and that interfering with the capacity of cSCC to secrete EVs inhibits tumor growth in vivo in a xenograft model of human cSCC. Transcriptome analysis of tumor xenografts by RNA-sequencing enabling the simultaneous quantification of both the human and the mouse transcripts revealed that impaired EV-production of cSCC cells prominently altered the phenotype of stromal cells, in particular genes related to extracellular matrix (ECM)-formation and epithelial-mesenchymal transition (EMT). In line with these results, co-culturing of human dermal fibroblasts (HDFs) with cSCC cells, but not with normal keratinocytes in vitro resulted in acquisition of cancer-associated fibroblast (CAF) phenotype. Interestingly, EVs derived from metastatic cSCC cells, but not primary cSCCs or NHEKs, were efficient in converting HDFs to CAFs. Multiplex bead-based flow cytometry assay and mass-spectrometry (MS)-based proteomic analyses revealed the heterogenous cargo of cSCC-derived EVs and that especially EVs derived from metastatic cSCCs carry proteins associated with EV-biogenesis, EMT, and cell migration. Mechanistically, EVs from metastatic cSCC cells result in the activation of TGFβ signaling in HDFs. Altogether, our study suggests that cSCC-derived EVs mediate cancer-stroma communication, in particular the conversion of fibroblasts to CAFs, which eventually contribute to cSCC progression.

| S-EPMC10372068 | biostudies-literature

Oncogenic ALKF1174L drives tumorigenesis in cutaneous squamous cell carcinoma

Project description:Cutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer characterized by increased mortality. Here, we show for the first time that anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase of the insulin receptor superfamily, plays a pivotal role in the pathogenesis of cSCC. Our data demonstrate that the overexpression of the constitutively active, mutated ALK, ALKF1174L is sufficient to initiate the development of cSCC and is 100% penetrant. Moreover, we show that cSCC development upon ALKF1174L overexpression is independent of the cell-of-origin. Molecularly, our data demonstrate that ALKF1174L cooperates with oncogenic KrasG12D and loss of p53, well established events in the biology of cSCC. This cooperation results in a more aggressive cSCC type associated with a higher-grade histological morphology. Finally, we demonstrate that Stat3 is a key downstream effector of ALKF1174L and is indispensable for ALKF1174L-driven cSCC tumorigenesis. In sum, these findings reveal that ALK can exert its tumorigenic potential via cooperation with multiple pathways crucial in the pathogenesis of cSCC. Finally, we show that human cSCCs contain mutations in the ALK gene. Taken together, our data identify ALK as a new key player in the pathogenesis of cSCC and this knowledge suggests that oncogenic ALK signaling can be a target for future clinical trials.

2020-04-15 | GSE147642 | GEO

Oncogenic ALKF1174L drives tumorigenesis in cutaneous squamous cell carcinoma

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

| PRJNA615866 | ENA

COL11A1 mutations in cutaneous squamous cell carcinoma [WES]

Project description:Whole exome sequencing was used to identify frequent COL11A1 mutations in cutaneous squamous cell carcinoma (cSCC).

2021-07-23 | GSE179296 | GEO

Differentially expressed miRNAs in human cutaneous squamous cell carcinoma

Project description:To determine the differentially expressed miRNAs in human cutaneous squamous cell carcinoma biopsies versus normal skin samples using microarray analysis.

2015-05-11 | E-MTAB-3409 | biostudies-arrayexpress

Oncogenic ALKF1174L drives tumorigenesis in cutaneous squamous cell carcinoma.

Project description:Cutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer characterized by increased mortality. Here, we show for the first time that anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase of the insulin receptor superfamily, plays a pivotal role in the pathogenesis of cSCC. Our data demonstrate that the overexpression of the constitutively active, mutated ALK, ALKF1174L , is sufficient to initiate the development of cSCC and is 100% penetrant. Moreover, we show that cSCC development upon ALKF1174L overexpression is independent of the cell-of-origin. Molecularly, our data demonstrate that ALKF1174L cooperates with oncogenic KrasG12D and loss of p53, well-established events in the biology of cSCC. This cooperation results in a more aggressive cSCC type associated with a higher grade histological morphology. Finally, we demonstrate that Stat3 is a key downstream effector of ALKF1174L and likely plays a role in ALKF1174L -driven cSCC tumorigenesis. In sum, these findings reveal that ALK can exert its tumorigenic potential via cooperation with multiple pathways crucial in the pathogenesis of cSCC. Finally, we show that human cSCCs contain mutations in the ALK gene. Taken together, our data identify ALK as a new key player in the pathogenesis of cSCC, and this knowledge suggests that oncogenic ALK signaling can be a target for future clinical trials.

| S-EPMC7184028 | biostudies-literature

Epigenome analysis of cutaneous squamous cell carcinoma samples

Project description:Genome wide DNA methylation profiling in cutaneous squamous cell carcinoma. The Infinium MethylationEPIC BeadChips 850K has been used to interrogate DNA methylation changes. The cohort included 23 patients in total, with precursors of squamous cell carcinoma (actinic keratosis group) and with cSCC at different stages.

2019-12-12 | E-MTAB-8542 | biostudies-arrayexpress

Characterisation of the adhesome of patient-derived cutaneous squamous carcinoma cells

Project description:Interactions between cells and the extracellular matrix, mediated by integrin adhesion complexes (IACs), play key roles in cancer progression and metastasis. We report here systems-level changes in the adhesome during progression of a patient-derived cutaneous squamous cell carcinoma (cSCC). We found that the actin regulatory protein Mena is enriched in IACs in metastatic cSCC cells and is connected within a subnetwork of actin-binding proteins to the LINC complex component nesprin-2.

2023-03-25 | PXD021492 | Pride

Long non-coding RNAs in cutaneous squamous cell carcinoma

Project description:The expression of lncRNAs in cutaneous squamous cell carcinoma (cSCC) were determined with a commercially available microarray (Arraystar Inc.,Rockville, Maryland USA). The Arraystar human lncRNA Microarray V3.0 containing 30,586 LncRNAs and 26,109 coding transcripts (mRNAs) A total of three patients with cSCC were biopsied. A total of three control (non-lesional skin) were biopsied.

2016-04-13 | E-GEOD-74859 | biostudies-arrayexpress

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