Wig1 prevents cellular senescence by regulating p21 mRNA decay through control of RISC recruitment

Kim, Bong Cho; Lee, Hyung Chul; Lee, Je Jung; Choi, Chang; Kim, Dong Kwan; Lee, Jae Cheol; Ko, Young Gyu; Lee, Jae Seon

doi:10.1038/emboj.2012.286

Cited by 33 publications

(38 citation statements)

References 52 publications

(71 reference statements)

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“…Blockade of ERN1 in glioma cells also leads to the decreased expression of ZMAT3 (TP53 target zinc finger protein) gene but molecular mechanisms of this relation is not yet clear. There is data that ZMAT3 participates in the TP53-dependent growth regulatory pathway by regulation of TP53 expression and translocation to the nucleus as well as RNA-mediated gene silencing [26,28,35]. At the same time, recently was shown that ZMAT3 as an mRNA stabilityregulating protein prevents cellular senescence [28] and its decrease possibly participate in suppression of ERN1 knockdown of glioma cells proliferation (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, SESN proteins provide an important link between genotoxic stress, TP53 and the mTOR signaling pathway. Recently was shown that ZMAT3 is an mRNA stability-regulating protein which prevents cellular senescence by regulating p21 mRNA decay through control of RISC recruitment [28]. ZMAT3 can bind different types of double-stranded RNAs, including small interfering RNAs and microRNAs [26,27].…”

Section: Introductionmentioning

confidence: 99%

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Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

Minchenko¹,

Danilovskyi²,

Kryvdiuk³

et al. 2014

Fiziol Zh

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Acute L-glutamine deprivation affects the expression of tP53-related protein genes in u87 glioma cells We have studied the effect of acute L-glutamine deprivation on the expression of tumor protein 53 (TP53)related genes such as TOPORS (topoisomerase I binding, arginine/serine-rich, E3 ubiquitin protein ligase), TP53BP1 (TP53 binding protein 1), TP53TG1 (TP53 inducible gene 1), SESN1 (p53 regulated PA26 nuclear protein), NME6 (NME/NM23 nucleoside diphosphate kinase 6), and ZMAT3 (zinc finger, Matrin-type 3) in glioma cells with ERN1 knockdown. It was shown that blockade of ERN1 function in U87 glioma cells is induced the expression of RYBP and SESN1 genes, but decreased the expression of TP53BP1, TP53TG1, TOPORS, NME6, genes. Moreover, the expression levels of RYBP, SESN1, TP53BP1, and ZMAT3 genes is increased in control glioma cells by L-glutamine deprivation condition but blockade of ERN1 signaling enzyme function significantly enhances this effect on the expression all of these genes. At the same time, the ERN1 knockdown eliminates the response TP53TG1 and TOPORS genes to L-glutamine deprivation condition. Results of this investigation clearly demonstrate that the expression most of genes encoding TP53-related factors depends upon acute L-glutamine deprivation condition as well as upon ERN1, the major signaling system of the endoplasmic reticulum stress.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

Minchenko¹,

Danilovskyi²,

Kryvdiuk³

et al. 2014

Fiziol Zh

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“…Xenograft mice were established as described previously. 72 In brief, a single-cell suspension of H460 cells (1 × 10 6 ) was injected subcutaneously into the lateral hind leg of 6-week-old BALB/c nude mice (n = 5). Average tumor volume was determined as (L × W 2 )/2; measurements of tumor length (L) and width (W) were taken with a caliper.…”

Section: Discussionmentioning

confidence: 99%

Heparan sulfation is essential for the prevention of cellular senescence

et al. 2015

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Cellular senescence is considered as an important tumor-suppressive mechanism. Here, we demonstrated that heparan sulfate (HS) prevents cellular senescence by fine-tuning of the fibroblast growth factor receptor (FGFR) signaling pathway. We found that depletion of 3′-phosphoadenosine 5′-phosphosulfate synthetase 2 (PAPSS2), a synthetic enzyme of the sulfur donor PAPS, led to premature cell senescence in various cancer cells and in a xenograft tumor mouse model. Sodium chlorate, a metabolic inhibitor of HS sulfation also induced a cellular senescence phenotype. p53 and p21 accumulation was essential for PAPSS2-mediated cellular senescence. Such senescence phenotypes were closely correlated with cell surface HS levels in both cancer cells and human diploid fibroblasts. The determination of the activation of receptors such as FGFR1, Met, and insulin growth factor 1 receptor β indicated that the augmented FGFR1/AKT signaling was specifically involved in premature senescence in a HS-dependent manner. Thus, blockade of either FGFR1 or AKT prohibited p53 and p21 accumulation and cell fate switched from cellular senescence to apoptosis. In particular, desulfation at the 2-O position in the HS chain contributed to the premature senescence via the augmented FGFR1 signaling. Taken together, we reveal, for the first time, that the proper status of HS is essential for the prevention of cellular senescence. These observations allowed us to hypothesize that the FGF/FGFR signaling system could initiate novel tumor defenses through regulating premature senescence.

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“…The vast majority of investigations into 3 ′ -UTR-mediated regulation has focused on isolated, individual elements within a 3 ′ UTR and have not determined how collections of elements might interact with one another. However, there exist a handful of examples of 3 ′ UTRs containing combinations of cis-regulatory elements that function cooperatively: Closely spaced binding sites for miRNAs can function synergistically, enhancing their regulatory impact (Grimson et al 2007;Saetrom et al 2007;Broderick et al 2011), and the binding of RBPs has been reported to both activate adjacent cryptic miRNA binding sites (Kim et al 2009(Kim et al , 2012Kedde et al 2010;Miles et al 2012) and mask otherwise functional sites (Bhattacharyya et al 2006;Kedde et al 2007;Léveillé et al 2011;Kundu, et al 2012). For example, two studies demonstrated that the binding of human Pumilio proteins within a 3 ′ UTR can induce a conformational change in the RNA structure.…”

Section: Introductionmentioning

confidence: 99%

Systematic analysis of the Hmga2 3′ UTR identifies many independent regulatory sequences and a novel interaction between distal sites

Kristjánsdóttir

Fogarty

Grimson

2015

RNA

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The 3 ′ untranslated regions (3 ′ UTRs) of mRNAs regulate transcripts by serving as binding sites for regulatory factors, including microRNAs and RNA binding proteins. Binding of such trans-acting factors can control the rates of mRNA translation, decay, and other aspects of mRNA biology. To better understand the role of 3 ′ UTRs in gene regulation, we performed a detailed analysis of a model mammalian 3′ UTR, that of Hmga2, with the principal goals of identifying the complete set of regulatory elements within a single 3 ′ UTR, and determining the extent to which elements interact with and affect one another. Hmga2 is an oncogene whose overexpression in cancers often stems from mutations that remove 3 ′ -UTR regulatory sequences. We used reporter assays in cultured cells to generate maps of cis-regulatory information across the Hmga2 3 ′ UTR at different resolutions, ranging from 50 to 400 nt. We found many previously unidentified regulatory sites, a large number of which were up-regulating. Importantly, the overall location and impact of regulatory sites was conserved between different species (mouse, human, and chicken). By systematically comparing the regulatory impact of 3 ′ -UTR segments of different sizes we were able to determine that the majority of regulatory sequences function independently; only a very small number of segments showed evidence of any interactions. However, we discovered a novel interaction whereby terminal 3 ′ -UTR sequences induced internal up-regulating elements to convert to repressive elements. By fully characterizing one 3 ′ UTR, we hope to better understand the principles of 3 ′ -UTR-mediated gene regulation.

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Wig1 prevents cellular senescence by regulating p21 mRNA decay through control of RISC recruitment

Cited by 33 publications

References 52 publications

Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells

Heparan sulfation is essential for the prevention of cellular senescence

Systematic analysis of the Hmga2 3′ UTR identifies many independent regulatory sequences and a novel interaction between distal sites

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