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Differentially expressed genes between YY1 knockdown and control cells, transfected in colorectal cancer cell line SW48

ABSTRACT: Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the oncological role of YY1 in CRC. To indentify the target genes of YY1, microarray analysis was performed on siYY1 and siControl transfected cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193949 | GEO | 2022/01/19

REPOSITORIES: GEO

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Differentially expressed genes between YY1 knockdown and control cells, transfected in colorectal cancer cell line DLD-1

Project description:Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the oncological role of YY1 in CRC. To indentify the target genes of YY1, microarray analysis was performed on siYY1 and siControl transfected cells.

2022-01-19 | GSE193948 | GEO

YY1 regulates DNA-DNA interaction

Project description:The DNA Guanine quadruplexes (G4) plays important roles in multiple cellular processes, including regulation of DNA replication, transcription and genome stability. Here, we show that Yin Yang-1 (YY1), a ubiquitously expressed and multifunctional transcription factor, can bind with G4 structures directly. Fluorescence anisotropy experiments shows that YY1 binds towards G4 structures with Kd in low nanomolar range (<100 nM) through the C terminal zinc finger domains. ChIP-seq results show that 81% of the YY1 ChIP-seq peaks contain G4 forming sequences, which is highly overlapped with the G4 ChIP-seq peaks. YY1 facilitate the DNA-DNA interaction through its binding with G4 structures in vivo and in vitro, which can be disturbed by G4 stabilizer treatment. In all, our studies identify a novel G4 structure binding protein-YY1, and reveal that G4 structure functions in DNA-DNA interaction.

2020-08-27 | GSE128106 | GEO

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

Project description:Analysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 3 months

2015-11-10 | E-GEOD-68429 | biostudies-arrayexpress

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

2015-11-10 | GSE68429 | GEO

Transcriptome Analysis Identifies Linc-Yy1, A Novel Functional LincRNA During Myogenesis

Project description:Little is known how lincRNAs are involved in skeletal myogenesis. Here we describe the discovery of a novel lincRNA, Linc-YY1 from the promoter of transcription factor (TF) Yin Yang 1 (YY1) gene. We demonstrate that Linc-YY1 is dynamically regulated during myogenesis in vitro and in vivo. Gain or loss of function of Linc-YY1 in C2C12 myoblast cells or satellite cells alters myogenic differentiation and in injured muscles impacts the course of regeneration. Further studies suggest LincYY1 may interact with YY1 through its middle domain to evict YY1

2015-10-16 | GSE74049 | GEO

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.

2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

Project description:Analysis of subcutaneous adipose tissue (IWAT) from Yin Yang 1 brown fat specific knockout mice fed a high fat diet for 2 weeks. The goal was to identify a gene signature of IWAT browning in YY1 mutant mice. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 2 weeks

2015-11-10 | E-GEOD-68382 | biostudies-arrayexpress

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

2015-11-10 | GSE68382 | GEO

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

2011-12-31 | GSE32238 | GEO

Epithelial inactivation of Yy1 abrogates lung branching morphogenesis

Project description:Yin Yang 1 (YY1) is a multifunctional zinc-finger-containing transcription factor that plays crucial roles in numerous biological processes by selectively activating or repressing transcription, depending upon promoter contextual differences and specific protein interactions. In mice, Yy1 null mutants die early in gestation while Yy1 hypomorphs die at birth from lung defects. We studied how the epithelial-specific inactivation of Yy1 impacts on lung development. The Yy1 mutation in lung epithelium resulted in neonatal death due to respiratory failure. It impaired tracheal cartilage formation, altered cell differentiation, abrogated lung branching, and caused airway dilation similar to those seen in human congenital cystic lung diseases. The cystic lung phenotype in Yy1 mutants can be explained by the reduced expression of Shh in lung endoderm, a transcriptional target of YY1, and the subsequent derepression of mesenchymal Fgf10 expression. Accordingly, SHH supplementation partially rescued the lung phenotype in vitro. Analysis of human lung tissues revealed decreased YY1 expression in children with pleuropulmonary blastoma (PPB), a rare pediatric lung tumor arising during fetal development and associated with DICER1 mutations. No evidence for a potential genetic interplay between murine Dicer and Yy1 genes during lung morphogenesis was observed. However, the cystic lung phenotype resulting from the epithelial inactivation of Dicer function mimics the Yy1 lung malformations with similar changes in Shh and Fgf10 expression. Together, our data demonstrate the critical requirement for YY1 in lung morphogenesis and identify Yy1 mutant mice as a potential model for studying the genetic basis of PPB.

2015-10-20 | GSE66171 | GEO

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