Cooperation between ARID3A and p53 in the transcriptional activation of p21WAF1 in response to DNA damage

Lestari, Widya; Ichwan, Solachuddin Jauhari Arief; Otsu, Megumi; Yamada, Seiichi; Iseki, Sachiko; Shimizu, Shihoko; Ikeda, Masa‐Aki

doi:10.1016/j.bbrc.2011.12.003

Cited by 24 publications

(18 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The AP1 complex, a known pro-inflammatory factor 17 , is particularly interesting in the light of our earlier findings that inflammation plays an important role in PAH 18,19 . Similarly, E4F1 and ARID3A have been shown to interact with and activate specific functions of p53 20,21 , which we have recently shown to be upregulated upon loss of BMPR2 in a process that is linked to the inflammasome 22 . CREB5 has been proposed as a hypoxia response gene in lung 23 , and its enhanced activity is likely a consequence of the disease.…”

Section: Extensive Remodeling Of H3k27ac In Pah Patients Vs Controlsmentioning

confidence: 69%

Remodeling of active endothelial enhancers is associated with aberrant gene-regulatory networks in pulmonary arterial hypertension

Reyes-Palomares

Grubert

et al. 2020

Nat Commun

View full text Add to dashboard Cite

Environmental and epigenetic factors often play an important role in polygenic disorders. However, how such factors affect disease-specific tissues at the molecular level remains to be understood. Here, we address this in pulmonary arterial hypertension (PAH). We obtain pulmonary arterial endothelial cells (PAECs) from lungs of patients and controls (n = 19), and perform chromatin, transcriptomic and interaction profiling. Overall, we observe extensive remodeling at active enhancers in PAH PAECs and identify hundreds of differentially active TFs, yet find very little transcriptomic changes in steady-state. We devise a disease-specific enhancer-gene regulatory network and predict that primed enhancers in PAH PAECs are activated by the differentially active TFs, resulting in an aberrant response to endothelial signals, which could lead to disturbed angiogenesis and endothelial-to-mesenchymaltransition. We validate these predictions for a selection of target genes in PAECs stimulated with TGF-β, VEGF or serotonin. Our study highlights the role of chromatin state and enhancers in disease-relevant cell types of PAH.

show abstract

Section: Extensive Remodeling Of H3k27ac In Pah Patients Vs Controlsmentioning

confidence: 69%

Remodeling of active endothelial enhancers is associated with aberrant gene-regulatory networks in pulmonary arterial hypertension

Reyes-Palomares

Grubert

et al. 2020

Nat Commun

View full text Add to dashboard Cite

show abstract

“…Neither cell cycle nor signature transcripts of these families were significantly altered in KO-MEFs (data not shown). However, that BRIGHT interacts with and is activated by p53 (Lestari et al., 2012), a previously established barrier to reprogramming (Li et al., 2009), suggests that Bright loss bypasses senescence through a mechanism other than transcriptional derepression of pluripotency factors, alleviating the requirement for derepression as the initiating step to reprogramming. Unlike loss or mutation of p53, Bright KO-MEFs do not undergo genomic instability at a level detectable by karyotype (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Bright/Arid3A Acts as a Barrier to Somatic Cell Reprogramming through Direct Regulation of Oct4, Sox2, and Nanog

et al. 2014

View full text Add to dashboard Cite

SummaryWe show here that singular loss of the Bright/Arid3A transcription factor leads to reprograming of mouse embryonic fibroblasts (MEFs) and enhancement of standard four-factor (4F) reprogramming. Bright-deficient MEFs bypass senescence and, under standard embryonic stem cell (ESC) culture conditions, spontaneously form clones that in vitro express pluripotency markers, differentiate to all germ lineages, and in vivo form teratomas and chimeric mice. We demonstrate that BRIGHT binds directly to the promoter/enhancer regions of Oct4, Sox2, and Nanog to contribute to their repression in both MEFs and ESCs. Thus, elimination of the BRIGHT barrier may provide an approach for somatic cell reprogramming.

show abstract

“…Although great efforts have been made in order to explore novel treatment approaches, there is not a significant difference in the overall survival of patients with OS in recent three to four decades (Xu et al, 2011). Previously, different studies used OS cells to elaborate the regulation of ARID3A by p53 (Lestari et al, 2012;Ma et al, 2003) and lncRNA ERICD by E2F1 (Feldstein et al, 2013). However, these studies did not highlight the function of ARID3A and ERICD in OS cells to a great extent.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells

Arman

Saadat

İğci³

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD.

show abstract

Cooperation between ARID3A and p53 in the transcriptional activation of p21WAF1 in response to DNA damage

Cited by 24 publications

References 19 publications

Remodeling of active endothelial enhancers is associated with aberrant gene-regulatory networks in pulmonary arterial hypertension

Remodeling of active endothelial enhancers is associated with aberrant gene-regulatory networks in pulmonary arterial hypertension

Bright/Arid3A Acts as a Barrier to Somatic Cell Reprogramming through Direct Regulation of Oct4, Sox2, and Nanog

Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells

Contact Info

Product

Resources

About