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MiRNAs in activated mouse CD4 T cells by Bcl-6 overexpression

ABSTRACT: Compare miRNA expression profiles in mouse CD4 T cells overexpression of Bcl-6 vs empty vector

ORGANISM(S): Mus musculus

PROVIDER: GSE17000 | GEO | 2009/07/24

SECONDARY ACCESSION(S): PRJNA117327

REPOSITORIES: GEO

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miRNAs in activated mouse CD4 T cells by Bcl-6 overexpression

Project description:Compare miRNA expression profiles in mouse CD4 T cells overexpression of Bcl-6 vs empty vector Mouse naÃ¯ve CD4+ T cells were transduced with a Bcl-6-expressing retrovirus or the control vector and cultured in Th0 condition for 2 days. Cells expressing medium to high levels of GFP were sorted and total RNAs were isolated using mirVana miRNA Isolation Kit (Applied Biosystems). MiRNA expression was profiled using Agilent 8x15K mouse miRNA microarray miRNA-v1_95_May07 (miRBase Release 9.2) by Ramaciotti Centre for Gene Function Analysis (Sydney). Each sample was run in duplicate.

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Expression data from BCL-3 overexpression HaCat cells

Project description:Constitutive activation of EGFR- and NF-kB-dependent pathways is a hallmark of cancer, yet signaling proteins that connect both oncogenic cascades are poorly characterized. Here we define KIAA1199 as a BCL-3- and p65-dependent gene in transformed keratinocytes. KIAA1199 expression is enhanced upon human papillomavirus (HPV) infection and is aberrantly expressed in clinical cases of cervical (pre)neoplastic lesions. Mechanistically, KIAA1199 binds Plexin A2 and protects from Semaphorin 3A-mediated cell death by promoting EGFR stability and signaling. Moreover, KIAA1199 is an EGFR-binding protein and KIAA1199 deficiency impairs EGF-dependent Src, MEK1 and ERK1/2 phosphorylations. Therefore, EGFR stability and signaling to downstream kinases requires KIAA1199. As such, KIAA1199 promotes EGF-mediated epithelial-mesenchymal transition (EMT). Taken together, our data define KIAA1199 as an oncogenic protein induced by HPV infection and constitutive NF-kB activity that transmits pro-survival and invasive signals through EGFR signaling. We used microarrays to detail the global programme of gene expression upon BCL-3 overexpression We used two experimental conditions, namely HaCat cells infected with a control lentivirus as well as HaCat cells infected with a BCL-3 expressing construct. Both experimental conditions were in triplicates.

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