Dataset Information

Effect of integrin α3β1 and/or integrin α9β1 expression on the mouse keratinocyte secretome

ABSTRACT: A parental immortalized mouse keratinocyte cell line which lacks integrin α3β1 and α9β1 were engineered to express either α3β1, α9β1, or α3β1 and α9β1 in combination. The conditioned medium from these cell lines were analyzed by MS/MS.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Keratinocyte

SUBMITTER: Scott Varney

LAB HEAD: Mike DiPersio

PROVIDER: PXD018425 | Pride | 2022-02-15

REPOSITORIES: Pride

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Publications

Integrin α3β1 on Tumor Keratinocytes Is Essential to Maintain Tumor Growth and Promotes a Tumor-Supportive Keratinocyte Secretome.

Longmate Whitney M WM Varney Scott S Power Derek D Miskin Rakshitha Pandulal RP Anderson Karl E KE DeFreest Lori L Van De Water Livingston L DiPersio C Michael CM

The Journal of investigative dermatology 20200523 1

The development of integrin-targeted cancer therapies is hindered by incomplete understanding of integrin function in tumor cells and the tumor microenvironment. Previous studies showed that mice with epidermis-specific deletion of the α3 integrin subunit fail to form skin tumors during two-step chemical tumorigenesis, indicating a protumorigenic role for integrin α3β1. Here, we generated mice with tamoxifen-inducible, epidermis-specific α3 knockout to determine the role of α3β1 in the maintenan ...[more]

PMID: 32454065

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Project description:Serum-driven responses, many of which are related to wound healing, are potentially deregulated in cancer development and associated genomic alterations might have prognostic value. The current study assessed fetal bovine serum-induced transcriptomic changes for clinical relevance in head and neck squamous cell carcinoma (HNSCC) using oral keratinocyte models otherwise routinely cultured without serum, including normal keratinocytes (NOK) and the transformed keratinocyte lines SVpgC2a, SqCC/Y1 and LK0412. Bioinformatics-driven analysis of gene expression implicated primarily serum-induced terminal differentiation in NOK including alterations in 99 genes, 13 gene ontology-categories and 6 molecular networks and involvement of 7 key regulator genes. Compared to NOK, the transformed lines expressed around 3-fold lower numbers of differently expressed transcripts, unique sets of gene ontologies, molecular networks and key regulator genes for each line, and consistent absence of terminal differentiation markers. Assessment of the complete in vitro/serum exposure-derived set of differentially expressed genes (totally 180 genes) relative a clinical, information-rich HNSCC data set identified 17 survival-associated genes of which only 12 had previous association to HNSCC. Multi-step validation of the survival-associated genes relative to several independent tumor data sets, including in the Human Gene Expression Map and Human Protein Atlas databases, confirmed novel association to HNSCC for genes COTL1 and INSIG1 and novel poor outcome prediction for the genes CUL4B and PDGFRL. The definition of normal and aberrant serum responses in keratinocyte models therefore coupled new genes to HNSCC including with relevance to prognosis. Analysis of gene expression changes in serum-exposed normal and transformed cells relative the respective un-exposed states. Significantly differentially expressed genes were next assessed by bioinformatics processing using Gene Ontology categories and network analyses. Findings were also validated relative independent HNSCC data sets as well as transcriptomics and proteomics databases.

Dataset Information

Effect of integrin α3β1 and/or integrin α9β1 expression on the mouse keratinocyte secretome

Publications

Integrin α3β1 on Tumor Keratinocytes Is Essential to Maintain Tumor Growth and Promotes a Tumor-Supportive Keratinocyte Secretome.

Similar Datasets

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