TIAF1 and p53 Functionally Interact in Mediating Apoptosis and Silencing of TIAF1 Abolishes Nuclear Translocation of Serine 15-Phosphorylated p53

Schultz, Lori; Khera, Smaira; Sleve, Daniel; Heath, John K.; Chang, Nan‐Shan

doi:10.1089/104454904322745943

Cited by 19 publications

(45 citation statements)

References 43 publications

(52 reference statements)

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“…Although TIAF1 (TGFB-1 induced antiapoptotic factor 1) interacts with TP53 in the cytosol and may participate in its nuclear translocation, TP53INP1 (TP53 inducible nuclear protein 1) is engaged in the regulation of TP53 activity in the nucleus [29,30]. Both TP53INP1 and TIAF1 genes were found to be overexpressed in the naturally occurring T Reg cells in our study.…”

Section: Resultsmentioning

confidence: 66%

Untitled

et al. 2006

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This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. T regulatory cell signatures

Comparison of the gene expression in human T regulatory cells and naïve cells using a T regulatory cell-specific microarray reveals cellspecific gene signatures.

Abstract Background: Naturally occurring CD4 + CD25 + regulatory T cells (T Reg ) are involved in the control of autoimmune diseases, transplantation tolerance, and anti-tumor immunity. Thus far, genomic studies on T Reg cells were restricted to murine systems, and requirements for their development, maintenance, and mode of action in humans are poorly defined.

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Section: Resultsmentioning

confidence: 66%

Untitled

et al. 2006

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Comparison of the gene expression in human T regulatory cells and naïve cells using a T regulatory cell-specific microarray reveals cellspecific gene signatures.

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“…UV light activates p53 and WOX1 in various cultured cell lines (25,29,38). Similarly, UV light rapidly induced p53 expression in the control cells but not in the WOX1si-expressing cells (Fig.…”

Section: Uv Light Does Not Induce P53 Expression In Wox1 Knockdownmentioning

confidence: 74%

WOX1 Is Essential for Tumor Necrosis Factor-, UV Light-, Staurosporine-, and p53-mediated Cell Death, and Its Tyrosine 33-phosphorylated Form Binds and Stabilizes Serine 46-phosphorylated p53

Chang

Doherty

Ensign

et al. 2005

Journal of Biological Chemistry

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116

270

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Hyaluronidases and hyaluronan are important mediators of tissue remodeling and cancer cell metastasis. Metastatic and malignant breast and prostate cancers frequently overexpress hyaluronidases and hyaluronan (1, 2). Hyaluronidases PH-20, Hyal-1, and Hyal-2 are known to induce the expression of a candidate tumor suppressor WW domaincontaining oxidoreductase WOX1 (also known as WWOX, FOR, or WWOXv1) (3-5).The human WWOX gene, which comprises nine exons encoding the WWOX/WOX1 family proteins, is located on a fragile site on the chromosome ch16q23.3-24.1 (6 -9). Eight mRNA transcripts of the WWOX gene have been found so far (7). However, it is still not known whether all of the mRNA transcripts are translated successfully into proteins. Isoforms WWOXv1 (46 kDa), WWOXv2 (42 kDa), and WWOXv8 (60 kDa) and several other small proteins can be found in normal and several types of cancer cells (3, 8 -11). 3 Genetic alterations of the WWOX gene and disappearance of WWOX/WOX1 family proteins have been shown in multiple types of cancers, especially at an invasive or a metastatic stage (8,9,(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). Hypermethylation of the WWOX gene may inactivate its expression (21). In contrast, significant up-regulation of WWOX/WOX1 family proteins has been shown during progression of breast, prostate and other cancers to a premetastatic state (10,22,23). Also, absent expression of these family proteins in metastatic cancer cells is not necessarily due to disruption of the WWOX gene. We have recently determined that post-transcriptional blockade of the fulllength mRNA translation to protein may account for the disappearance of the WWOX/WOX1 family proteins in cutaneous squamous cell carcinoma cells in patients and in UVB-treated mice (24).Wild type WOX1 possesses two N-terminal WW domains (containing conserved tryptophan residues), a nuclear localization sequence and a C-terminal short-chain alcohol dehydrogenase/reductase domain (which contains a mitochondria-targeting sequence) (3). Sex steroid hormones such as estrogen and androgen activate WOX1 via Tyr 33 phosphorylation (p-WOX1) and nuclear translocation (11). Importantly, p-WOX1 is located in the mitochondria during benign prostatic hypertrophy (11). Nuclear translocation of p-WOX1 occurs when prostate cells progress toward cancerous and metastatic states (11), suggesting a critical role of WOX1 phosphorylation during prostate cancer development.We determined that WOX1 enhances the cytotoxic function of tumor necrosis factor (TNF) 4 and induces apoptosis when overexpressed (3). We also showed that in response to stress or apoptotic stimuli, WOX1 becomes phosphorylated at Tyr 33 , which allows its complex formation with activated p53 and JNK1 (25). The p53-WOX1 complex translocates to the mitochondria and nuclei to mediate apoptosis (25,26). WOX1 induces apoptosis synergistically with p53 (3,25). In contrast, JNK1 may block WOX1-induced cell death (25). Src is known to phosphorylate WOX1 at Tyr 33 (27). We also determined that Tyr 33 -phosphorylated WO...

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“…For chromosome 3p12.1, the breakpoint mapped to the 3 der (3) der (17) 17 3 der (3) der (17) RP11-331K15 clone, giving signals on normal chromosome 3, on derivative der(3), and on derivative der (17). Using a similar strategy, we were also able to map the chromosome 17q11.2 breakpoint to the BAC clone RP11-321A17 (AC024619).…”

Section: Breakpoint Characterizationmentioning

confidence: 92%

“…Somatic cell hybrids from the patient's lymphoblasts were generated to separate the normal chromosomes 3 and 17 and the two derivative chromosomes der(3) and der (17). DNA from these hybrids was used in a PCR-based strategy with selected non-polymorphic markers spanning the region defined by BAC clones (not shown).…”

Section: Breakpoint Characterizationmentioning

confidence: 99%

“…15 -16 It has also been shown that TIAF1 and p53 functionally interact in regulating apoptosis, and TIAF1 is likely to participate in the nuclear translocation of activated p53. 17 The role of TIAF1 in preventing cellular apoptosis is very intriguing in the light of the patient's HSCR phenotype as it has been hypothesized that one of the causes of HSCR pathogenesis is a defect in normal survival of enteric neurons and/or premature apoptosis. 1 The expression profile of the MYO18A and TIAF genes performed on a panel of 24 human tissues is in agreement with literature data, showing a quite ubiquitous presence of the two genes with a preferential expression in the muscle (data not shown).…”

Section: Breakpoint Characterizationmentioning

confidence: 99%

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Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

Griseri¹,

Vos

Giorda

et al. 2008

Eur J Hum Genet

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Hirschsprung's disease (HSCR), a congenital complex disorder of intestinal innervation, is often associated with other inherited syndromes. Identifying genes involved in syndromic HSCR cases will not only help understanding the specific underlying diseases, but it will also give an insight into the development of the most frequent isolated HSCR. The association between hydrocephalus and HSCR is not surprising as a large number of patients have been reported to show the same clinical association, most of them showing mutations in the L1CAM gene, encoding a neural adhesion molecule often involved in isolated X-linked hydrocephalus. L1 defects are believed to be necessary but not sufficient for the occurrence of the intestinal phenotype in syndromic cases. In this paper, we have carried out the molecular characterization of a patient affected with Hirschsprung's disease and X-linked hydrocephalus, with a de novo reciprocal balanced translocation t(3;17)(p12;q21). In particular, we have taken advantage of this chromosomal defect to gain access to the predisposing background possibly leading to Hirschsprung's disease. Detailed analysis of the RET and L1CAM genes, and molecular characterization of MYO18A and TIAF1, the genes involved in the balanced translocation, allowed us to identify, besides the L1 mutation c.2265delC, different additional factors related to RET-dependent and -independent pathways which may have contributed to the genesis of enteric phenotype in the present patient.

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TIAF1 and p53 Functionally Interact in Mediating Apoptosis and Silencing of TIAF1 Abolishes Nuclear Translocation of Serine 15-Phosphorylated p53

Cited by 19 publications

References 43 publications

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WOX1 Is Essential for Tumor Necrosis Factor-, UV Light-, Staurosporine-, and p53-mediated Cell Death, and Its Tyrosine 33-phosphorylated Form Binds and Stabilizes Serine 46-phosphorylated p53

Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

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