Expression of TCF3 target genes defines a subclass of diffuse large B-cell lymphoma characterized by up-regulation of MYC target genes and poor clinical outcome following R-CHOP therapy
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PROVIDER: PRJNA874036 | ENA |
REPOSITORIES: ENA
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Project description:Fifty-eight retrospectively-ascertained local cases of diffuse large B-cell lymphoma (DLBCL) were segregated into two large subgroups with divergent overall survival through expression profiling of 135 transcripts including 92 regulated downstream of TCF3 or recurrently mutated in DLBCL or Burkitt lymphoma
2022-11-10 | GSE212114 | GEO
Project description:We report the direct target genes of ATF4 and CHOP in response to endoplasim reticulum stress through next generation sequencing. By obtaining genowide sequence from chromatin immunoprecipitated DNA with anti-CHOP and anit-ATF4, we identified direct binding sites of ATF4 and CHOP in promoter regions of their target genes in mouse embrynic fibroblasts (MEFs) in response to ER stress. In addition, we obtained list of genes which are differentially regulated in Atf4 or Chop-deficient MEFs compared to the wild-type MEFs in response to ER stress. We found that genes related with unfolded protein response and protein synthesis were directly regulated by ATF4 and CHOP. Through this observation, we conclude that main role of ATF4 and CHOP as transcription factors is to enhance mRNA translation in respone to ER stress. This sutdy provide new insight of genetic network of ATF4 and CHOP in response to ER stress.
2013-04-11 | GSE35681 | GEO
Project description:We report the direct target genes of ATF4 and CHOP in response to endoplasim reticulum stress through next generation sequencing. By obtaining genowide sequence from chromatin immunoprecipitated DNA with anti-CHOP and anit-ATF4, we identified direct binding sites of ATF4 and CHOP in promoter regions of their target genes in mouse embrynic fibroblasts (MEFs) in response to ER stress. In addition, we obtained list of genes which are differentially regulated in Atf4 or Chop-deficient MEFs compared to the wild-type MEFs in response to ER stress. We found that genes related with unfolded protein response and protein synthesis were directly regulated by ATF4 and CHOP. Through this observation, we conclude that main role of ATF4 and CHOP as transcription factors is to enhance mRNA translation in respone to ER stress. This sutdy provide new insight of genetic network of ATF4 and CHOP in response to ER stress. For ChIP-seq, Chop+/+ and Chop-/- MEFs were treated with Tunicamycin, N-glycosylation inhibitor, to induce ER stress for 8hr. Atf4+/+ and Atf4-/- MEFs were also treated same condition for ChIP-Seq. For mRNA-seq, wild-type, Atf4-/-, and Chop-/- MEFs were treated with tunicamycin for 8hr for experiments.
2013-04-11 | E-GEOD-35681 | biostudies-arrayexpress
Project description:The observation that Tcf3 (MGI name: Tcf7l1) bound the same genes as core stem cell transcription factors, Oct4 (MGI name:Pou5f1), Sox2 and Nanog, revealed a potentially important aspect of the poorly understood mechanism whereby Wnts stimulate self renewal of pluripotent mouse embryonic stem (ES) cells. Although the conventional view of Tcf proteins as the β-catenin-binding effectors of Wnt signaling suggested Tcf3 should activate target genes in response to Wnts, here we show that Wnt3a and Tcf3 effectively antagonize each other’s effects on gene expression. Genetic ablation of Tcf3 caused similar effects as treating cells with recombinant Wnt3a. Moreover, Tcf3 was not necessary for Wnt3a-stimulation of gene expression as the majority of Wnt3a-stimulated genes exhibited a greater increase in Tcf3-/- ES cells than in Tcf3+/+ ES cells. These expression data, together with genetic experiments, show that Wnt3a stimulates ES cell self renewal by inhibiting Tcf3.
2011-02-24 | GSE27455 | GEO
Project description:The observation that Tcf3 (MGI name: Tcf7l1) bound the same genes as core stem cell transcription factors, Oct4 (MGI name:Pou5f1), Sox2 and Nanog, revealed a potentially important aspect of the poorly understood mechanism whereby Wnts stimulate self renewal of pluripotent mouse embryonic stem (ES) cells. Although the conventional view of Tcf proteins as the β-catenin-binding effectors of Wnt signaling suggested Tcf3 should activate target genes in response to Wnts, here we show that Wnt3a and Tcf3 effectively antagonize each other’s effects on gene expression. Genetic ablation of Tcf3 caused similar effects as treating cells with recombinant Wnt3a. Moreover, Tcf3 was not necessary for Wnt3a-stimulation of gene expression as the majority of Wnt3a-stimulated genes exhibited a greater increase in Tcf3-/- ES cells than in Tcf3+/+ ES cells. These expression data, together with genetic experiments, show that Wnt3a stimulates ES cell self renewal by inhibiting Tcf3. Tcf3+/+ and Tcf3-/- mouse embryonic stem cells were cultured in self renewal conditions containing recombinant Wnt3a for RNA extraction and hybridization on Affymetrix microarrays.
2011-02-24 | E-GEOD-27455 | biostudies-arrayexpress
Project description:Regulatory factors controlling stem cell identity and self-renewal are often active in aggressive cancers and are thought to promote their growth and progression. TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem (ES) cell identity. We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferentially of the basal-like subtype. This suggested that TCF3 is involved in the regulation of breast cancer cell differentiation state and tumorigenicity. Silencing of TCF3 dramatically decreased the ability of breast cancer cells to initiate tumor formation, and led to decreased tumor growth rates. In culture, TCF3 promotes the sphere formation capacity of breast cancer cells and their self-renewal. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells, while repressing another distinct target subset. In the normal mouse mammary gland Tcf3 is highly expressed in terminal end buds, structures that lead duct development. Primary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the developing gland disrupts ductal growth. Our results identify TCF3 as a central regulator of tumor growth and initiation, and a novel link between stem cells and cancer.
2012-10-23 | GSE38893 | GEO
Project description:Regulatory factors controlling stem cell identity and self-renewal are often active in aggressive cancers and are thought to promote their growth and progression. TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem (ES) cell identity. We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferentially of the basal-like subtype. This suggested that TCF3 is involved in the regulation of breast cancer cell differentiation state and tumorigenicity. Silencing of TCF3 dramatically decreased the ability of breast cancer cells to initiate tumor formation, and led to decreased tumor growth rates. In culture, TCF3 promotes the sphere formation capacity of breast cancer cells and their self-renewal. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells, while repressing another distinct target subset. In the normal mouse mammary gland Tcf3 is highly expressed in terminal end buds, structures that lead duct development. Primary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the developing gland disrupts ductal growth. Our results identify TCF3 as a central regulator of tumor growth and initiation, and a novel link between stem cells and cancer. Cells infected with different shRNA vectors were either untreated, treated with control or Wnt3A condition medium. Condition medium treatments were done in biological repeats.
2012-10-23 | E-GEOD-38893 | biostudies-arrayexpress
Project description:Wnt/-catenin signaling controls self-renewal and pluripotency maintenance in both embryonic and adult stem cells (SCs) in mouse. We show that the activation of Wnt pathway drastically reduces proliferation of mESCs by direct binding of the the Wnt-effector Tcf1 to directly binds and regulates the Ink4/Arf locus , thereby Wnt pathway activation drastically reduces proliferation of mESCs and its regulation. We have conducted ChipSeq experiments for Tcf1 and Tcf3 with background to identify the genome wide binding locations Tcf1 and Tcf3 in mouse ESC.
2017-03-14 | E-MTAB-4358 | biostudies-arrayexpress
Project description:Identification of target genes of the transcription factors TCF1 and TCF3 in mouse embryonic stem cells (ChIP-Seq)
| PRJEB12564 | ENA