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Expression data from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 mouse embryos

ABSTRACT: The transcription factor Sox11 is a crucial regulator of kidney development. It is expressed in both mesenchymal and epithelial components of the early kidney anlagen. Deletion of Sox11 in mice causes an extension of the domain expressing Gdnf within rostral regions of the nephrogenic cord and results in duplex kidney formation. To gain insight into potential targets we performed microarray analysis on RNA isolated from the caudal region of E10.75 wildtype and mutant nephrogenic cords. 281 probe sets presented statistically significant changes (76 up, 205 down; FDR<0.1)

ORGANISM(S): Mus musculus

PROVIDER: GSE105426 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA415168

REPOSITORIES: GEO

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Expression data from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 mouse embryos

Project description:Expression data from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 mouse embryos

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SOX11-SMARCA4 Complex Drives Oncogenic Gene Regulation in Mantle Cell Lymphoma

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Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL). We have recently demonstrated SOX11 tumorigenic potential in vivo by showing a significant reduction on tumor growth of SOX11-knockdown MCL cells in xenograft experiments, confirming the clinical observations that SOX11 may play an important role in the aggressive behavior of MCL (Vegliante et al., 2013). However, the specific mechanisms regulated by SOX11 that promote the oncogenic and rapid tumor growth of aggressive MCL still remain to be elucidated. To further characterize the potential oncogenic mechanisms regulated by SOX11 in MCL, we have analyzed the GEP derived from the xenograft SOX11-positive and knockdown xenograft derived tumors. Differential gene expression between SOX11-positive Z138 and SOX11-negative Z138 MCL cell lines xenotransplanted in SCID mices derived tumors. To determine the transcriptional programs regulated by SOX11 we first generated a MCL cellular model with reduced SOX11 protein levels by infecting MCL cell lines with lentiviral particles carrying shRNA plasmids specifically targeting SOX11 (shSOX11.1 and shSOX11.3). Next, CB17-severe combined immunodeficient (CB17-SCID) mice (Charles River Laboratory, Wilmington, MA) were subcutaneously inoculated into their lower dorsum with Z138 shSOX11.1, shSOX11.3, shControl in Matrigel basement membrane matrix and compared the GEP of SOX11-positive and SOX11-negative MCL xenotransplant derived tumors using the Affymetrix U133+2.0 microarrays.

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SOX11 Gene Expression Profiling

Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL), but its functional role in malignant B-cells is unknown. To identify target genes transcriptionally regulated by SOX11 in malignant lymphoid cells, we have used Gene Expression Profiling (GEP) after SOX11 silencing in MCL cell lines. Differential gene expression between Z138-shSOX11 and Z138-shControl MCL cell lines. To determine the transcriptional programs regulated by SOX11, we first generated an MCL cellular model with reduced SOX11 protein levels by infecting MCL cell lines with lentiviral particles carrying shRNA plasmids specifically targeting SOX11 (shSOX11.1 and shSOX11.3). Next, we compared the GEP of shSOX11 and shControl Z138 stable transduced clones using the Affymetrix U133+2.0 microarrays.

2013-04-04 | E-GEOD-34763 | biostudies-arrayexpress

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Project description:To identify potential SOX11 target genes in myxoid liposarcoma (MLS) we stably transfected codon optimized full-length human SOX11 into the SOX11 negative MLS cell line MLS-1765. An emtpy vector (EV) was used as control. Potential SOX11 target genes were correlated with data set GSE52390.

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Sox11 loss-of-function mutant cortex at E17.5

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SOX11 promotes skin fibrosis by inducing fibrotic factors

Project description:In this study, we demonstrated that baseline SOX11 expression was significantly higher in dermal fibroblasts (DFs) isolated from patients with SSc than that in controls, and increased in response to TGF-b. We then showed that SOX11 is involved in the expression of periostin and some periostin-dependent fibrotic factors identified in lung fibroblasts previously. Moreover, we identified some fibrotic factors induced by SOX11 in DNA microarrays combining TGF-b induction and SOX11 knockdown. Finally, we showed that genetic deletion of SOX11 in Postn positive fibroblast cells protects from bleomycin (BLM)-induced skin fibrosis. Altogether, our data indicate that SOX11 and periostin forms a vicious circle and that TGF-b activates this circle specifically in SSc dermal fibroblasts.

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