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Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE84194 | GEO | 2017/02/09

SECONDARY ACCESSION(S): PRJNA328257

REPOSITORIES: GEO

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Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate [mouse RNA-Seq]

Project description:Cutaneous squamous cell carcinoma (cuSCC) comprises 15-20% of all skin cancers, accounting for over 700,000 cases in the U.S. annually. Most cuSCC arise in association with a distinct precancerous lesion, the actinic keratosis (AK). In order to identify potential targets for molecularly targeted chemoprevention, we performed integrated cross-species genomic analysis of cuSCC development through the preneoplastic AK stage using matched human samples and a solar UV-driven Hairless mouse model. We identified the major transcriptional drivers of this sequence showing that the key genomic changes in cuSCC development occur in the normal skin to AK transition. Our data validate the use of this UV-driven mouse cuSCC model for cross-species analysis and demonstrate that cuSCC bears deep molecular similarities to multiple carcinogen-driven SCCs from diverse sites, suggesting that cuSCC may serve as an effective, accessible model for multiple SCC types and that common treatment and prevention strategies may be feasible.

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Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate [human miRNA-Seq]

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Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate [mouse miRNA-Seq]

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Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate

Project description:Identification of transcriptomic drivers of squamous cell carcinoma development through a preneoplastic intermediate

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Cross-species identification of genomic drivers of squamous cell carcinoma development across preneoplastic intermediates.

Project description:Cutaneous squamous cell carcinoma (cuSCC) comprises 15-20% of all skin cancers, accounting for over 700,000 cases in USA annually. Most cuSCC arise in association with a distinct precancerous lesion, the actinic keratosis (AK). To identify potential targets for molecularly targeted chemoprevention, here we perform integrated cross-species genomic analysis of cuSCC development through the preneoplastic AK stage using matched human samples and a solar ultraviolet radiation-driven Hairless mouse model. We identify the major transcriptional drivers of this progression sequence, showing that the key genomic changes in cuSCC development occur in the normal skin to AK transition. Our data validate the use of this ultraviolet radiation-driven mouse cuSCC model for cross-species analysis and demonstrate that cuSCC bears deep molecular similarities to multiple carcinogen-driven SCCs from diverse sites, suggesting that cuSCC may serve as an effective, accessible model for multiple SCC types and that common treatment and prevention strategies may be feasible.

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Integrative genomic characterization of oral squamous cell carcinoma identifies frequent somatic drivers

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Identification of potential gene drivers of cutaneous squamous cell carcinoma: Analysis of microarray data.

Project description:Cutaneous squamous cell carcinoma (cSCC) is a common skin cancer with an increasing incidence. As a pre-cancerous condition, actinic keratosis (AK) has an up to 20% risk of progression to cSCC. This study aims to define the potential genes that associated with genesis and progression of cSCC, thereby further identify critical biomarkers for the prevention, early diagnosis, and effective treatment of cSCC.Two datasets GSE42677 and GSE45216 were downloaded from the GEO. Microarray data analysis was applied to explore the differentially expressed genes (DEGs) between cSCC samples and AK samples. Then functional enrichment analysis, protein-protein interaction (PPI) network, and drug-gene interaction analysis were performed to screen key genes.A total of 711 DEGs, including 238 upregulated genes and 473 downregulated genes, were screened out. DEGs mainly involved in pathways as extracellular matrix (ECM)-receptor interaction, hematopoietic cell lineage, phosphatidylinositol 3-kinase (PI3K-Akt) signaling pathway, and focal adhesion. Candidate genes, including upregulated genes as JUN, filamin A (FLNA), casein kinase 1 delta (CSNK1D), and histone cluster 1 H3 family member f (HIST1H3F), and downregulated genes as androgen receptor (AR), heat shock protein family H member 1 (HSPH1), tropomyosin 1 (TPM1), pyruvate kinase, muscle (PKM), LIM domain and actin binding 1 (LIMA1), and synaptopodin (SYNPO) were screened out. In drug-gene interaction analysis, 13 genes and 44 drugs were identified.This study demonstrates that genes JUN, FLNA, AR, HSPH1, and CSNK1D have the potential to function as targets for diagnosis and treatment of cSCC.

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Project description:Cutaneous squamous cell carcinoma (cuSCC) is the second most common skin cancer and commonly arises in chronically UV-exposed skin or chronic wounds. Since UV exposure and chronic wounds are the two most prominent environmental factors that lead to cuSCC initiation, we undertook this study to test whether more acute molecular responses to UV and wounding overlapped with molecular signatures of cuSCC. We reasoned that transcriptional signatures in common between acutely UV-exposed skin, wounded skin, and cuSCC tumors, might enable us to identify important pathways contributing to cuSCC. We performed transcriptomic analysis on acutely UV-exposed human skin and integrated those findings with datasets from wounded skin and our transcriptomic data on cuSCC using functional pair analysis, GSEA, and pathway analysis. Integrated analyses revealed significant overlap between these three datasets, thus highlighting deep molecular similarities these biological processes, and we identified Oncostatin M (OSM) as a potential common upstream driver. Expression of OSM and its downstream targets correlated with poorer overall survival in head and neck SCC patients. In vitro, OSM promoted invasiveness of keratinocytes and cuSCC cells and suppressed apoptosis of irradiated keratinocytes. Together, these results support the concept of using an integrated, biologically-informed approach to identify potential promoters of tumorigenesis.

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