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Suppression of SOX7 by DNA methylation and its tumor suppressor function in acute myeloid leukemia

ABSTRACT: SOX7 was commonly downregulated in AML by hypermethylation. Re-expression of SOX7 in AML reduced the survival of AML

ORGANISM(S): Homo sapiens

PROVIDER: GSE67817 | GEO | 2015/04/14

SECONDARY ACCESSION(S): PRJNA280988

REPOSITORIES: GEO

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Suppression of SOX7 by DNA methylation and its tumor suppressor function in acute myeloid leukemia

Project description:SOX7 was commonly downregulated in AML by hypermethylation. Re-expression of SOX7 in AML reduced the survival of AML Overexpression of GFP-SOX7 by lenti-viral transduction in 3 AML cell lines and compared the expression level of genes normalized to GFP control

2015-04-14 | E-GEOD-67817 | biostudies-arrayexpress

Regulation of p21 by TWIST2 contributes to its tumor suppressor function in human acute myeloid leukemia

Project description:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML)M-BM- patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray. 4 independent biological replicates of control and TWIST2 expressed THP-1 cells have been used for RNA extraction and microarray analysis with Agilent platform.

2014-05-07 | E-GEOD-57347 | biostudies-arrayexpress

Regulation of p21 by TWIST2 contributes to its tumor suppressor function in human acute myeloid leukemia

Project description:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML) patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray.

2014-05-07 | GSE57347 | GEO

Sox7 regulates lineage decisions in cardiovascular progenitor cells

Project description:Specification of the mesodermal lineages requires a complex set of morphogenetic events orchestrated by interconnected signaling pathways and gene regulatory networks. The transcription factor Sox7 has critical functions in differentiation of multiple mesodermal lineages, including cardiac, endothelial, and hematopoietic. Using a doxycycline-inducible mouse embryonic stem cell (mESC) line, we have previously shown that expression of Sox7 in cardiovascular progenitor cells promotes expansion of endothelial progenitor cells. Here, we show that the ability of Sox7 to promote endothelial cell fate occurs at the expense of the cardiac lineage. Using ChIP-Seq coupled with ATAC-Seq we identify downstream target genes of Sox7 in cardiovascular progenitor cells and, by integrating these data with transcriptomic analyses, we define Sox7-dependent gene programs specific to cardiac and endothelial progenitor cells. Further, we demonstrate a protein-protein interaction between SOX7 and GATA4 and provide evidence that Sox7 interferes with the transcriptional activity of Gata4 on cardiac genes. In addition, we show Sox7 modulates WNT and BMP signaling during cardiovascular differentiation. Our data represent the first genome-wide analysis of Sox7 function and reveal a critical role for Sox7 in regulating signaling pathways that affect cardiovascular progenitor cell differentiation.

2019-07-06 | GSE133899 | GEO

SOX7 ChIP-seq in HUVECs

Project description:We investigated SOX7 binding events on the chromatin under basal conditions in human umbilical vein endothelial cells, upon overexpression of human SOX7-mCherry and immunoprecipitating mCherry. Cells overexpressing only the mCherry tag were used as negative control condition, and peaks called here were substracted from the SOX7-mCherry peaks.

2017-02-01 | E-MTAB-4480 | biostudies-arrayexpress

Gata6 induced XEN-like cells w/o Sox7

2015-09-14 | GSE66971 | GEO

SOX7 Target Genes and their Contribution to its Tumor Suppressive Function

Project description:As a transcription factor, SOX7 suppresses cancer development. However, only a few genes were demonstrated as SOX7-activated targets in cancer-irrelevant contexts. We used microarray chips to determine SOX7 target genes in breast cancer cells and discovered multiple signaling pathways altered by ectopic SOX7. We also investigated several genes for their roles in SOX7-mediated tumor suppression. Our study innovatively revealed SOX7 target gene profile in a cancer-relevant context and identified several SOX7-repressed target genes.

2018-02-26 | GSE111122 | GEO

Gata6 induced XEN-like cells w/o Sox7

Project description:To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern. Sox7 (+/-) ES cells and Sox7 (-/-) ES cells are forced to differentiate into XEN-like cells by Gata6-GR transgene. To compare the gene expression, we collected RNA samples at day4 with or without dexamethasone treatment from each genotype.

2015-09-14 | E-GEOD-66971 | biostudies-arrayexpress

HUVEC gene profile after Sox7/Sox17 siRNA silencing

Project description:To find out the target of transcription factor Sox7 and Sox17, DNA microarray analysis was performed with RNA from Sox7 and Sox17 knockdown HUVECs.

2016-11-23 | GSE75380 | GEO

SOX7 regulates MAPK/ERK-BIM mediated apoptosis in cancer cells

Project description:Here we showed that SOX7 was significantly downregulated in different cancer types, especially in lung and breast cancers. Low expression of SOX7 was associated with advanced stage of cancer with shorter overall survival. Cancer cells with loss of SOX7 promoted cell survival and colony formation, suppressed cellular apoptosis and produced a drug resistant phenotype against a variety of chemo/targeting therapeutic agents. Mechanistically, SOX7 induced cellular apoptosis through upregulation of genes associated with both P38 and apoptotic signaling pathway, as well as preventing the proteasome mediated degradation of pro-apoptotic protein BIM. Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation.

2022-05-08 | GSE130917 | GEO

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