Hepatic ARID3A facilitates liver cancer malignancy by cooperating with CEP131 to regulate an embryonic stem cell-like gene signature
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE193726 | GEO | 2022/08/10
REPOSITORIES: GEO
Similar Datasets
Project description:In order to determine proteins interacting with ARID3A in the ML-DS cell line CMK, we performed CoIP of endogenous ARID3A followed by LC-MS/MS
2023-03-11 | PXD025027 | Pride
Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina
2016-07-01 | E-GEOD-79638 | biostudies-arrayexpress
Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs.
2016-07-01 | GSE79638 | GEO
Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a ChIP was performed using bioChIP-sequencing. Control ChIP-sequencing was performed using BirA cells. HDAC1 ChIP was performed as native antibody ChIP-sequencing.
2014-10-16 | E-GEOD-56876 | biostudies-arrayexpress
Project description:To analyze the role of Fus, Ewsr1, and Taf15 in alternative RNA processing, we performed exon array analysis in N2A cells using exon arrays. N2A cells were transfected with siRNA using Lipofectamine RNAiMAX (Life Technologies) according to the manufacturer’s instructions.
2020-08-10 | GSE60694 | GEO
Project description:To test the function and regulated genes of ARID3A gene, we conducted lentivirus-mediated short hairpin RNA (shRNA) against ARID3A in K562 cell line.
2023-06-01 | E-MTAB-12603 | biostudies-arrayexpress
Project description:Percentages of ARID3a-expressing low density neutrophils in SLE patients correlate with lupus disease activity and Type I IFN production. ARID3a protein levels also correlate with interferon expression in plasmacytoid dendritic cells. Gene profiles mechanistically link ARID3a with inflammatory pathway regulation.
2018-09-26 | GSE117836 | GEO
Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a overexpression and Arid3a knockdown Total RNA was isolated from cultured cells using RNeasy plus mini kit (Qiagen). cDNA were synthesized and labelled, followed by hybridization on Affymetrix GeneChip mouse genome 430A 2.0 arrays.
2014-10-16 | E-GEOD-56853 | biostudies-arrayexpress
Project description:Using a siRNA screen we identified the histone demethylase enzyme KDM3A as a potential positive regulator of ER signalling in breast cancer. To interrogate the full extent of KDM3A regulation on ER signalling we assessed basal and estrogen (E2)- stimulated global gene expression changes in KDM3A-depleted MCF-7 cells by microarray analysis using the Illumina Human HT12 Version 4 BeadChip array. We identified ER regulated genes affected by KDM3A knockdown and determined that KDM3A is required for ER recruitment to estrogen response elements in the promotors of ER regulated genes. We also identified that KDM3A regulates expression of a number of genes involved in proliferation and that knockdown of KDM3A inhibits ER positive breast cancer cell growth. MCF-7 cells were transfected with either a non-silencing scrambled control siRNA (siSCR) or a KDM3A targeting siRNA (siKDM3A-B) using Lipfectamine RNAiMAX (Invitrogen) to a final concentration of 25 nM in steroid depleted conditions. Cells were grown for 48 hours prior to treatment with vehicle or 10 nM E2 for 4 hours before RNA extraction using TRIzol (Ambion, Life Technologies) and hybridization of triplicate samples to an Illumine HT-12 v4 BeadChip array. One sample failed due to low amounts of cRNA and was therefore not included in the analysis (siKDM3A + E2 Replicate 3). The array for replicates 1 and 2 was performed in August 2013 (Array 1) and replicate 3 in August 2014 (Array 2). When processing the data Array 2 was normalized to Array 1.
2015-05-16 | E-GEOD-68918 | biostudies-arrayexpress
Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification.
2014-10-16 | GSE56853 | GEO