TRIM8 modulates p53 activity to dictate cell cycle arrest

Caratozzolo, Mariano Francesco; Micale, Lucia; Turturo, Maria Giuseppina; Cornacchia, S; Fusco, Carmela; Marzano, Flaviana; Augello, Bartolomeo; D’Erchia, Anna Maria; Guerrini, Luisa; Pesole, Graziano; Sbisà, Elisabetta; Merla, Giuseppe; Tullo, Apollonia

doi:10.4161/cc.11.3.19008

Cited by 58 publications

(77 citation statements)

References 36 publications

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“…TRIM8 interacts with and negatively regulates PIAS3, a protein inhibitor of IL-6-dependent activation of STAT3, a signaling pathway important for cancer development and progression [6]. In agreement with previously data, we recently reported TRIM8 as a new modulator of the p53-mediated tumor suppression mechanism [7]. Under stress conditions, such as UV exposure, we showed that p53 induces the expression of TRIM8, which in turn stabilizes p53 leading to cell cycle arrest and reduction of cell proliferation through enhancement of p21 and GADD45 expression [7].…”

Section: Introductionsupporting

confidence: 85%

TRIM8 downregulation in glioma affects cell proliferation and it is associated with patients survival

et al. 2015

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BackgroundHuman gliomas are a heterogeneous group of primary malignant brain tumors whose molecular pathogenesis is not yet solved. In this regard, a major research effort has been directed at identifying novel specific glioma-associated genes. Here, we investigated the effect of TRIM8 gene in glioma.MethodsTRIM8 transcriptional level was profiled in our own glioma cases collection by qPCR and confirmed in the independent TCGA glioma cohort. The association between TRIM8 expression and Overall Survival and Progression-free Survival in TCGA cohort was determined by using uni-multivariable Cox regression analysis. The effect of TRIM8 on patient glioma cell proliferation was evaluated by performing MTT and clonogenic assays. The mechanisms causing the reduction of TRIM8 expression were explored by using qPCR and in vitro assays.ResultsWe showed that TRIM8 expression correlates with unfavorable clinical outcome in glioma patients. We found that a restored TRIM8 expression induced a significant reduction of clonogenic potential in U87MG and patient’s glioblastoma cells. Finally we provide experimental evidences showing that miR-17 directly targets the 3′ UTR of TRIM8 and post-transcriptionally represses the expression of TRIM8.ConclusionsOur study provides evidences that TRIM8 may participate in the carcinogenesis and progression of glioma and that the transcriptional repression of TRIM8 might have potential value for predicting poor prognosis in glioma patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1449-9) contains supplementary material, which is available to authorized users.

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Section: Introductionsupporting

confidence: 85%

TRIM8 downregulation in glioma affects cell proliferation and it is associated with patients survival

et al. 2015

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“…Indeed, TRIM24 (Allton et al, 2009), TRIM39 (Zhang et al, 2012a,b) and TRIM59 (Zhou et al, 2014) help to degrade p53. In addition, TRIM8, TRIM13, TRIM19, TRIM21 and TRIM25 also affect p53 stability (Bernardi et al, 2004;Joo et al, 2011;Caratozzolo et al, 2012;Reddy et al, 2014;Zhang et al, 2015). TRIM28, TRIM29 and TRIM32 antagonize p53 function (Wang et al, 2005;Yuan et al, 2010;Liu et al, 2014).…”

Section: Role Of Trim-directed Precision Autophagy In Diseasementioning

confidence: 99%

Precision autophagy directed by receptor regulators – emerging examples within the TRIM family

Kimura

Mandell

Deretić

2016

Journal of Cell Science

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Selective autophagy entails cooperation between target recognition and assembly of the autophagic apparatus. Target recognition is conducted by receptors that often recognize tags, such as ubiquitin and galectins, although examples of selective autophagy independent of these tags are emerging. It is less known how receptors cooperate with the upstream autophagic regulators, beyond the well-characterized association of receptors with Atg8 or its homologs, such as LC3B (encoded by MAP1LC3B), on autophagic membranes. The molecular details of the emerging role in autophagy of the family of proteins called TRIMs shed light on the coordination between cargo recognition and the assembly and activation of the principal autophagy regulators. In their autophagy roles, TRIMs act both as receptors and as platforms ('receptor regulators') for the assembly of the core autophagy regulators, such as ULK1 and Beclin 1 in their activated state. As autophagic receptors, TRIMs can directly recognize endogenous or exogenous targets, obviating a need for intermediary autophagic tags, such as ubiquitin and galectins. The receptor and regulatory features embodied within the same entity allow TRIMs to govern cargo degradation in a highly exact process termed 'precision autophagy'.

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“…9,10 Second, p53 binding partners, such as Hzf, Slug and hCAS, selectively regulate the expression of cell cycle arrest genes or apoptotic genes. [11][12][13][14] Third, some p53 targets, for example Glx2 (also called glyoxalase II) and Cdkn1a, regulate the survival of cells after DNA damage but do not affect the expression of other p53 targets. 15 Last, the levels of p53 in response to stresses also affect the outcome of various stresses.…”

Section: Rap2b a Novel P53 Target Regulates P53-mediated Pro-survivmentioning

confidence: 99%

Rap2b, a novel p53 target, regulates p53-mediated pro-survival function

Zhang

Lee

et al. 2013

Cell Cycle

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TRIM8 modulates p53 activity to dictate cell cycle arrest

Abstract: A novel p53-inducible gene, PAG608, encodes a nuclear zinc finger protein whose overexpression promotes apoptosis interactions between p53 and these genes are generally

Cited by 58 publications

References 36 publications

TRIM8 downregulation in glioma affects cell proliferation and it is associated with patients survival

TRIM8 downregulation in glioma affects cell proliferation and it is associated with patients survival

Precision autophagy directed by receptor regulators – emerging examples within the TRIM family

Rap2b, a novel p53 target, regulates p53-mediated pro-survival function

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