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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (NHLF cells)

ABSTRACT: We sought to dissect SOX11-dependent and -independent genes in IL-13–inducible genes in primary human lung fibroblasts

ORGANISM(S): Homo sapiens

PROVIDER: GSE104937 | GEO | 2018/08/02

REPOSITORIES: GEO

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Hierarchical control of interleukin 13 (IL-13) signals in lung fibroblasts by STAT6 and SOX11.

Project description:Interleukin (IL)-13 is a signature cytokine of type 2 inflammation important for the pathogenesis of various diseases, including allergic diseases. Signal transducer and activator of transcription (STAT) 6 is a critical transcriptional factor for the IL-13 signals; however, it remains unknown how expression of the IL-13-induced genes is differentiated by the transcriptional machineries. In this study, we identified IL-13-induced transcriptional factors in lung fibroblasts using DNA microarrays in which SOX11 was included. Knockdown of SOX11 down-regulated expression of periostin and CCL26, both of which are known to be downstream molecules of IL-13, whereas enforced expression of SOX11 together with IL-13 stimulation enhanced expression of periostin. Moreover, we found that in DNA microarrays combining IL-13 induction and SOX11 knockdown there exist both SOX11-dependent and -independent molecules in IL-13-inducible molecules. In the former, many inflammation-related and fibrosis-related molecules, including periostin and CCL26, are involved. These results suggest that SOX11 acts as a trans-acting transcriptional factor downstream of STAT6 and that in lung fibroblasts the IL-13 signals are hierarchically controlled by STAT6 and SOX11.

| S-EPMC6153291 | biostudies-literature

Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (NHLF cells)

Project description:Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (NHLF cells)

| PRJNA414194 | ENA

Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-08-02 | GSE104938 | GEO

Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts

Project description:Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

Project description:To identify candidates for trans-acting factors for IL-13–induced genes in lung fibroblasts, we searched transcriptional factors among IL-13–inducible molecules in lung fibroblasts

2018-08-02 | GSE104936 | GEO

Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

Project description:Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

| PRJNA414195 | ENA

SOX11-positive and SOX11-knockdown xenograft derived tumor Gene Expression Profilings

2014-11-04 | GSE52892 | GEO

SOX11-positive and SOX11-knockdown xenograft derived tumor Gene Expression Profilings

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.

2014-11-04 | E-GEOD-52892 | biostudies-arrayexpress

Clinicopathological features and prognostic value of SOX11 in childhood acute lymphoblastic leukemia

Project description:Acute lymphoblastic leukemia is marked by aberrant transcriptional features that alter cell differentiation, self-renewal, and proliferative features. We sought to identify the transcription factors exhibiting altered and subtype-specific expression patterns in B-ALL and report here that SOX11, a developmental and neuronal transcription factor, is aberrantly expressed in the ETV6-RUNX1 and TCF3-PBX1 subtypes of acute B-cell leukemias. We show that a high expression of SOX11 leads to alterations of gene expression that are typically associated with cell adhesion, migration, and differentiation. A high expression is associated with DNA hypomethylation at the SOX11 locus and a favorable outcome. The results indicate that SOX11 expression marks a group of patients with good outcomes and thereby prompts further study of its use as a biomarker.

2018-12-18 | GSE123943 | GEO

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.

2013-04-04 | GSE34763 | GEO

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