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Transcriptional profiling of SmoM2 expressing IFE cells at different stages of basal cell carcinoma formation

ABSTRACT: Basal cell carcinoma initiating cells undergo profound and rapid reprogramming into embryonic hair follicle progenitor like fate upon SmoM2 expression. Activation of Wnt/β-catenin signaling pathways is required in a cell autonomous manner for the reprogramming of adult IFE progenitors into EHFP-like fate as well as for tumor initiation. We used MA to define the molecular changes that occur in basal cell carcinoma initiating cells form the first oncogenic hit to the development of invasive tumor and further on to investigate the role of Wnt/β-catenin signaling activation in molecular changes occurring early during BCC development.

ORGANISM(S): Mus musculus

PROVIDER: GSE40612 | GEO | 2012/09/06

SECONDARY ACCESSION(S): PRJNA174398

REPOSITORIES: GEO

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Project description:Tumor: tumor microenvironment (TME) interactions are critical for tumor progression and the composition and structure of the local extracellular matrix (ECM) are key determinants of tumor metastasis. We recently reported that activation of Wnt/beta- catenin signaling in Ewing sarcoma cells induces widespread transcriptional changes that are associated with acquisition of a metastatic tumor phenotype. Significantly, ECM protein-encoding genes were found to be enriched among Wnt/beta-catenin induced transcripts, leading us to hypothesize that activation of canonical Wnt signaling might induce changes in the Ewing sarcoma secretome. To address this hypothesis, conditioned media from Ewing sarcoma cell lines cultured in the presence or absence of Wnt3a was collected for proteomic analysis. Label-free mass spectrometry was used to identify and quantify differentially secreted proteins. We then used in silico databases to identify only proteins annotated as secreted. Comparison of the secretomes of two Ewing sarcoma cell lines revealed numerous shared proteins, as well as a degree of heterogeneity, in both basal and Wnt-stimulated conditions. Gene set enrichment analysis of secreted proteins revealed that Wnt stimulation reproducibly resulted in increased secretion of proteins involved in ECM organization, ECM receptor interactions, and collagen formation. In particular, Wnt-stimulated Ewing sarcoma cells upregulated secretion of structural collagens, as well as matricellular proteins, such as the metastasis-associated protein, tenascin C (TNC). Interrogation of published databases confirmed reproducible correlations between Wnt/beta-catenin activation and TNC and COL1A1 expression in patient tumors. In summary, this first study of the Ewing sarcoma secretome reveals that Wnt/beta-catenin activated tumor cells upregulate secretion of ECM proteins. Such Wnt/beta-catenin mediated changes are likely to impact on tumor: TME interactions that contribute to metastatic progression.

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Transcriptional profiling of SmoM2 expressing IFE cells at different stages of basal cell carcinoma formation

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