Share this article Share with email Share with twitter Share with linkedin Share with facebook. Interestingly, in these cancer cells, Triad 1-induced apoptosis is not mediated by Gfi-1 stabilization but is instead pdependent.
Moreover, Triad 1 promotes transactivation of p These results suggest that Triad 1 can induce apoptosis through its ligase activity via p53 activation.
Full text links Read article at publisher's site DOI : References Articles referenced by this article 27 p death star. Wild-type p53 activates transcription in vitro. Ubiquitin-mediated regulation of apoptosis. The E3 ubiquitin-protein ligase Triad1 inhibits clonogenic growth of primary myeloid progenitor cells. Gfi1 ubiquitination and proteasomal degradation is inhibited by the ubiquitin ligase Triad1.
Gfi-1 restricts proliferation and preserves functional integrity of haematopoietic stem cells. The growth factor independence-1 transcription factor: new functions and new insights. The Gfi-1 protooncoprotein represses Bax expression and inhibits T-cell death. Show 10 more references 10 of Smart citations by scite. The number of the statements may be higher than the number of citations provided by EuropePMC if one paper cites another multiple times or lower if scite has not yet processed some of the citing articles.
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E3 ubiquitin ligase Hades negatively regulates the exonuclear function of p The pinducible E3 ubiquitin ligase p53RFP induces pdependent apoptosis. WW domain-containing E3 ubiquitin protein ligase 1 targets p63 transcription factor for ubiquitin-mediated proteasomal degradation and regulates apoptosis.
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Contact us Privacy Terms of use Copyright Accessibility. Quite frequently, when two proteins bind reaching a maximal strength, the protein complex further drives to polymerization and leads to aggregation for causing apoptosis [ 22 , 23 , 24 , 28 ]. We demonstrated for the first time that there is a functional antagonism between these two tumor suppressors. However, p53 abolishes the function of WWOX in causing cancer-mediated inflammation.
For unknown reasons, the growing tumors induce protein aggregation in the mouse brain and lung. We believe that cytokines released by growing cancer cells induce protein aggregation. The observations indicate there is an ongoing neurodegeneration in the brain of tumor-growing mice. We have recently shown that growing melanoma or glioblastoma in mice leads to neurodegeneration [ 26 ]. How the tumor cells in the flanks control neurodegeneration in the brain is unknown and remains to be established.
TIAF1 is a potential tumor suppressor. We demonstrated the anticancer function of TIAF1 by showing its critical role in cell death. TIAF1 is upregulated in growing tumors, but may disappear in established metastatic cancer cells [ 23 , 28 ].
TIAF1 protein aggregation has been shown in the human cortex and hippocampus of nondemented mid-aged humans and demented old patients [ 22 , 24 , 25 , 26 ]. Also, TIAF1 and amyloid fibrils are significantly accumulated in the stroma of progressing lung cancer cells [ 23 ].
These peritumor materials probably provide support for cancer cell survival. Together, our previous and current findings imply that Smad4 and p53 restrict TIAF1 self-aggregation, and that loss of tumor suppressors p53, WWOX, and Smad4 results in TIAF1 aggregate formation, which supports cancer growth and causes neurodegeneration. Summary illustration. All data generated or analyzed during this study are included in this article and the supplementary material.
Exp Biol Med. WWOX tumor suppressor gene in breast Cancer, a historical perspective and future directions. Front Oncol. Article Google Scholar. WWOX phosphorylation, signaling, and role in neurodegeneration. Front Neurosci. Tanna M, Aqeilan RI. Modeling WWOX loss of function in vivo: what have we learned?
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Sci Rep. Nat Genet. Biochim Biophys Acta Rev Cancer. The supposed tumor suppressor gene WWOX is mutated in an early lethal microcephaly syndrome with epilepsy, growth retardation and retinal degeneration. Orphanet J Rare Dis. Cell Death Dis. TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in pdeficient environment, and cell death. Chang J, Chang N. Cell Death Discov. Alzheimers Dement N Y.
Google Scholar. A missense mutation in TRAPPC6A leads to build-up of the protein, in patients with a neurodevelopmental syndrome and dysmorphic features. Self-aggregating TIAF1 in lung cancer progression. Transl Respir Med. Hyaluronidase induction of a WW domain-containing oxidoreductase that enhances tumor necrosis factor cytotoxicity. WOX1 is essential for tumor necrosis factor-, UV light-, staurosporine-, and pmediated cell death, and its tyrosine phosphorylated form binds and stabilizes serine phosphorylated p World J Gastroenterol.
BMC Biol. PubMed Google Scholar. Chasing the signaling run by tri-molecular time-lapse FRET microscopy. TIAF1 and p53 functionally interact in mediating apoptosis and silencing of TIAF1 abolishes nuclear translocation of serine phosphorylated p DNA Cell Biol.
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Cloning and characterization of a novel transforming growth factor-beta1-induced TIAF1 protein that inhibits tumor necrosis factor cytotoxicity. J Cell Biol. Cold Spring Harb Perspect Med. Vieler M, Sanyal S. Cancers Basel. Mamm Genome. Down-regulation of WW domain-containing oxidoreductase induces tau phosphorylation in vitro.
A potential role in Alzheimer's disease. J Cell Biochem. Int J Mol Sci. Deciphering p53 signaling in tumor suppression. Curr Opin Cell Biol. Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound. Nat Med. Chang NS. The non-ankyrin C terminus of Ikappa Balpha physically interacts with p53 in vivo and dissociates in response to apoptotic stress, hypoxia, DNA damage, and transforming growth factor-beta 1-mediated growth suppression.
Strategies by which WWOX-deficient metastatic cancer cells utilize to survive via dodging, compromising, and causing damage to WWOX-positive normal microenvironment. Xing J, Liu C. Identification of genes associated with histologic tumor grade of esophageal squamous cell carcinoma. Download references. You can also search for this author in PubMed Google Scholar. P-YC carried out cell migration assays, time-lapse microscopy, apoptosis assay, gene cloning, transforming growth on agarose, and immunofluorescence microscopy, and wrote thesis for her Master degree as part of this manuscript.
S-RL and M-HL performed gene cloning, plasmid purification, apoptosis assay, and transforming growth on agarose. LS carried out transforming growth on agarose. C-IS proofread the manuscript. N-SC conceived ideas, carried out promoter activation assay, FRET microscopy, co-immunoprecipitation, and yeast two-hybrid analysis, and wrote and revised the manuscript for submission.
All authors read and approved the final manuscript. Correspondence to Nan-Shan Chang. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Figure S1. The image is digitally enlarged from Fig. Figure S2. WWOX-deficient cells have a faster migration rate.
This data links to Fig. Figure S3. Figure S4. Figure S5. The image data is enlarged from Fig. Figure S6. Data is shown as an average of duplicate experiments. This data supports Fig. PDF kb. Video S1. Following removal of the culture-insert, cells were allowed to migrate to each other from both sides.
MP4 kb. Video S2. Reprints and Permissions. Chou, PY. Cell Commun Signal 17, 76 Download citation. Received : 08 February Accepted : 04 June Published : 17 July Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.
Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Methods Time-lapse microscopy was used to measure the extent of cell migration. Results Wwox -deficient MEF cells exhibited constitutive Smad3 and p38 activation and migrated individually and much faster than wild type cells.
Cell migration assay, promoter activation, and time-lapse microscopy Cell migration assay was performed as described [ 24 ]. Cell cycle analysis Cells were electroporated with indicated EGFP-tagged plasmids and cultured overnight. Soft agarose colony survival assay Adherence-independent cell growth or transforming growth was performed in a soft agarose colony survival assay [ 40 ]. Full size image.
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