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Of the 34 undifferentiated endometrial carcinomas examined, 17 (50%) exhibited SWI (zeige SMARCA1 ELISA Kits)/SNF (zeige SNRPA ELISA Kits) complex inactivation, with 11 tumors showing complete loss of both ARID1A and ARID1B (zeige ARID1B ELISA Kits), 5 showing complete loss of BRG1 (zeige SMARCA4 ELISA Kits) and 1 showing complete loss of INI1 (zeige SMARCB1 ELISA Kits). Ten of the remaining 17 undifferentiated carcinomas showed the following alterations: 5 tumors (15%) showed loss of ARID1A only with intact ARID1B (zeige ARID1B ELISA Kits), BRG1 (zeige SMARCA4 ELISA Kits), and INI1 (zeige SMARCB1 ELISA Kits) expression.
BAF250a loss in AE is consistently associated with the development of BAF250a-negative endometriosis-associated cancers and appears to be an early event in most of these cases.
Transcriptome analysis revealed ARID1A knockdown led to miR-503 upregulation. CDKN2A was identified as a target of miR-503, which contributes to cell senescence. Thus, the data suggests that ARID1A deficiency promote KRAS(G12D)-driven pancreatic tumorigenesis through miR-503/CDKN2A-mediated senescence.
ARID1A may be a primary driver of carcinogenesis in a subset of esophageal adenocarcinomas
ARID1A mutation inactivates the apoptosis-promoting function of p53 (zeige TP53 ELISA Kits) by upregulating HDAC6 (zeige HDAC6 ELISA Kits), indicating that pharmacological inhibition of HDAC6 (zeige HDAC6 ELISA Kits) is a therapeutic strategy for ARID1A-mutated cancers.
ARID1A mutation can be an early stage event in the oncogenic transformation of endometriosis cells giving rise to ovarian clear cell carcinoma.
ARID1A expression is significantly decreased in higher stages of urothelial carcinoma and its aggressive variants.
Our data suggests that deficiency or loss of functional mutations of ARID1A in HCC (zeige FAM126A ELISA Kits) cells might contribute to the increased activity of certain cancer-promoting lncRNAs.
ARID1A loss lacks prognostic significance in early stage colorectal adenocarcinoma.
ARID1A may play an important role in the early events of gastric carcinogenesis.
Mice with liver-specific homozygous or heterozygous Arid1a loss were resistant to tumor initiation while ARID1A overexpression accelerated initiation.
Loss of HDAC (zeige HDAC3 ELISA Kits)-mediated repression and gain of NF-kappaB (zeige NFKB1 ELISA Kits) activation underlie cytokine induction in ARID1A- and PIK3CA (zeige PIK3CA ELISA Kits)-mutation-driven ovarian cancer.
ARID1A normally targets SWI (zeige SMARCA1 ELISA Kits)/SNF (zeige SNRPA ELISA Kits) complexes to enhancers.
Consistent with the latter, Arid1a reexpression in tumor cells led to increased p21 (Cdkn1a (zeige CDKN1A ELISA Kits)) expression and dramatic accumulation of cells in G2 phase of the cell cycle. These results also indicate a potential opportunity for therapeutic intervention in ARID1A-deficient human breast cancer subtypes that retain one intact copy of the gene and also maintain wild-type TRP53 (zeige TP53 ELISA Kits) activity
The Arid1a loss reprograms chromatin to restrict promoter access by transcription factors such as C/ebpalpha (zeige CEBPA ELISA Kits), which enforces differentiation, and E2F4 (zeige E2F4 ELISA Kits), which suppresses cell-cycle re-entry.
This study provides an alternative mechanism by which Arid1a deficiency contributes to hepatocellular carcinoma tumorigenesis.
ARID1A positively regulates Klf15 (zeige KLF15 ELISA Kits) expression with PGR (zeige PGR ELISA Kits) to inhibit epithelial proliferation at peri (zeige POSTN ELISA Kits)-implantation. Our results suggest that Arid1a has a critical role in modulating epithelial proliferation which is a critical requisite for fertility
Our results indicate that the Arid1a tumour suppressor gene has a key role in regulating ovarian endometrioid carcinoma differentiation
ARID1A and PIK3CA (zeige PIK3CA ELISA Kits) mutations cooperate to promote tumour growth through sustained IL-6 (zeige IL6 ELISA Kits) overproduction.
This gene encodes a member of the SWI/SNF family, whose members have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The encoded protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin. It possesses at least two conserved domains that could be important for its function. First, it has a DNA-binding domain that can specifically bind an AT-rich DNA sequence known to be recognized by a SNF/SWI complex at the beta-globin locus. Second, the C-terminus of the protein can stimulate glucocorticoid receptor-dependent transcriptional activation. It is thought that the protein encoded by this gene confers specificity to the SNF/SWI complex and may recruit the complex to its targets through either protein-DNA or protein-protein interactions. Two transcript variants encoding different isoforms have been found for this gene.
ARID domain-containing protein 1A
, AT-rich interactive domain-containing protein 1A
, BRG1-associated factor 250a
, OSA1 nuclear protein
, SWI-like protein
, SWI/SNF complex protein p270
, SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin subfamily F member 1
, brain protein 120
, chromatin remodeling factor p250
, osa homolog 1
, AT rich interactive domain 1A (Swi1 like)
, BRG1-associated factor 250
, SWI-SNF complex protein p270
, SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily f, member 1
, Swi1 like
, AT rich interactive domain 1A (SWI-like)
, AT-rich interactive domain-containing protein 1A-like