TIF1γ Suppresses Tumor Progression by Regulating Mitotic Checkpoints and Chromosomal Stability

Pommier, Roxane M.; Gout, Johann; Vincent, David F.; Alcaraz, Lindsay B.; Chuvin, Nicolas; Arfi, Vanessa; Martel, Sylvie; Kaniewski, Bastien; Devailly, Guillaume; Fourel, Geneviève; Bernard, Pascal; Moyret‐Lalle, Caroline; Ansieau, Stéphane; Puisieux, Alain; Valcourt, Ulrich; Sentis, Stéphanie; Bartholin, Laurent

doi:10.1158/0008-5472.can-14-3426

Cited by 30 publications

(37 citation statements)

References 52 publications

(75 reference statements)

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“…The chick embryo model has been widely used to study the metastatic spread of human cancer cells after they are directly injected intravenously into the chorioallantoic membrane. In addition to higher throughput, the chick embryo model has several advantages over mouse models ( Lokman et al ., 2012 ), and, of importance, results obtained using this system have been shown to replicate those derived from mouse models ( Azoitei et al ., 2014 ; Pommier et al ., 2015 ; Virtakoivu et al ., 2015 ). To facilitate the detection of metastases, we infected 231-CTR or 231-oxSNX9 cells with retroviruses driving the stable expression of zsGreen.…”

Section: Resultsmentioning

confidence: 99%

SNX9 promotes metastasis by enhancing cancer cell invasion via differential regulation of RhoGTPases

Bendris

Williams²,

Reis

et al. 2016

MBoC

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Section: Resultsmentioning

confidence: 99%

SNX9 promotes metastasis by enhancing cancer cell invasion via differential regulation of RhoGTPases

Bendris

Williams²,

Reis

et al. 2016

MBoC

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“…TRIM33 inactivation has been shown to lead to chromosomal defects, and reduced TRIM33 expression correlated with an increased rate of genomic rearrangements (201). Accordingly, TRIM33 down-regulation is connected to various forms of cancer, most notably chronic myelomonocytic leukemia (202) and hepatocellular carcinoma (203).…”

Section: Degradation Impaired Through Decreased E3 Ligase Activitymentioning

confidence: 99%

Degrons in cancer

et al. 2017

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Degrons are the elements that are used by E3 ubiquitin ligases to target proteins for degradation. Most degrons are short linear motifs embedded within the sequences of modular proteins. As regulatory sites for protein abundance, they are important for many different cellular processes, such as progression through the cell cycle and monitoring cellular hypoxia. Degrons enable the elimination of proteins that are no longer required, preventing their possible dysfunction. Although the human genome encodes~600 E3 ubiquitin ligases, only a fraction of these enzymes have well-defined target degrons. Thus, for most cellular proteins, the destruction mechanisms are poorly understood. This is important for many diseases, especially for cancer, a disease that involves the enhanced expression of oncogenes and the persistence of encoded oncoproteins coupled with reduced abundance of tumor suppressors. Lossof-function mutations occur in the degrons of several oncoproteins, such as the transcription factors MYC and NRF2, and in various mitogenic receptors, such as NOTCH1 and several receptor tyrosine kinases. Mutations eliminating the function of the b-catenin degron are found in many cancers and are considered one of the most abundant mutations driving carcinogenesis. In this Review, we describe the current knowledge of degrons in cancer and suggest that increased research on the "dark degrome" (unknown degron-E3 relationships) would enhance progress in cancer research.

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“…Also, it binds multiple chromatin sites in monocyte to promote production of macrophage, binds other chromatin sites in mature macrophage to regulate the responses after toll-like receptor (TLR) activation by lipo-polysaccharide (LPS) ( 111 ), and is directly involved in proteasome activation via the ubiquitination of DHX33 ( 112 ). TIF1γ also has many roles in cell homeostasis; TIF1γ is strongly involved in antiproliferative cellular effect by (i) mediating ubiquitination and then the degradation of LIM-domain-binding protein which is involved in the transcription of cycle activator genes ( 113 ) and (ii) interaction with APC/C (anaphase-promoting complex/cyclosome) to promote the alignment and stability of chromosomes during mitosis and to prevent abnormal metaphase–anaphase transition ( 75 , 76 ). Moreover, TIF1γ is largely involved in DNA repair by recruiting different proteins promoting chromatin relaxation and repair ( 114 , 115 ).…”

Section: Targets Of Cancer-associated Autoimmune Response In Myositismentioning

confidence: 99%

Dermatomyositis and Immune-Mediated Necrotizing Myopathies: A Window on Autoimmunity and Cancer

2017

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Autoimmune myopathies (myositides) are strongly associated with malignancy. The link between myositis and cancer, originally noticed by Bohan and Peter in their classification in 1975 (1), has been evidenced by large population-based cohort studies and a recent meta-analysis. The numerous reports of cases in which the clinical course of myositis reflects that of cancer and the short delay between myositis and cancer onset support the notion that myositis may be an authentic paraneoplastic disorder. Thus, cancer-associated myositis raises the question of cancer as a cause rather than a consequence of autoimmunity. Among myositides, dermatomyositis and more recently, although to a lesser extent, immune-mediated necrotizing myopathies are the most documented forms associated with cancer. Interestingly, the current diagnostic approach for myositis is based on the identification of specific antibodies where each antibody determines specific clinical features and outcomes. Recent findings have shown that the autoantibodies anti-TIF1γ, anti-NXP2 and anti-HMGCR are associated with cancers in the course of myositis. Herein, we highlight the fact that the targets of these three autoantibodies involve cellular pathways that intervene in tumor promotion and we discuss the role of cancer mutations as autoimmunity triggers in adult myositis.

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TIF1γ Suppresses Tumor Progression by Regulating Mitotic Checkpoints and Chromosomal Stability

Cited by 30 publications

References 52 publications

SNX9 promotes metastasis by enhancing cancer cell invasion via differential regulation of RhoGTPases

SNX9 promotes metastasis by enhancing cancer cell invasion via differential regulation of RhoGTPases

Degrons in cancer

Dermatomyositis and Immune-Mediated Necrotizing Myopathies: A Window on Autoimmunity and Cancer

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