The ubiquitin-like modifier FAT10 in cancer development. (October 2016)

• Record Type: Journal Article
• Authors: Aichem, Annette; Groettrup, Marcus
• Is Part Of: International journal of biochemistry & cell biology. Volume 79(2016:Oct.)
• Page Start: 451
• Page End: 461
• Publication Date: 2016-10
• Subjects: AIPL1 aryl-hydrocarbon receptor like-1 -- APC/C anaphase-promoting complex/cyclosome -- DUB deubiquitylating enzyme -- EMT epithelial-mesenchymal transition -- FAT10 HLA-F adjacent transcript 10 -- GSK glycogen synthase kinase -- HCC hepatocellular carcinoma -- HLA human leukocyte antigen -- HOX homeobox -- IFN interferon -- IL interleukin -- MAD2 mitotic arrest deficient 2 -- mTEC medullary thymic epithelial cells -- NF-κB nuclear factor kappa-B -- NUB1L NEDD8-ultimate buster 1 long -- STAT signal transducer and activator of transcription -- SUMO small-ubiquitin-like modifier -- TGF transforming growth factor -- TNF tumor necrosis factor -- UBD Ubiquitin D -- ULM ubiquitin-like modifier -- UPS ubiquitin proteasome system -- USE1 UBA6-specific E2 enzyme 1; FAT10 -- UBD -- Inflammation -- Ubiquitin proteasome system -- Carcinogenesis; Biochemistry -- Periodicals; Cytology -- Periodicals; Biochemistry -- Periodicals; Cell Biology -- Periodicals; Biochimie -- Périodiques; Cytologie -- Périodiques; Biochimie; Cytologie; Biochemistry; Cytology; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); Periodicals; 572.05
• DOI: 10.1016/j.biocel.2016.07.001
• Languages: English
• ISSNs: 1357-2725

Abstract

Graphical abstract: Highlights: The ubiquitin-like modifier FAT10 is an autonomous signal for proteasomal degradation. FAT10 is overepressed in numerous cancer types. FAT10 expression promotes carcinogenic properties. FAT10 binds to MAD2, p53, and β-catenin. First mechanisms of FAT10-mediated tumor promotion revealed. Abstract: During the last years it has emerged that the ubiquitin-like modifier FAT10 is directly involved in cancer development. FAT10 expression is highly up-regulated by pro-inflammatory cytokines IFN-γ and TNF-α in all cell types and tissues and it was also found to be up-regulated in many cancer types such as glioma, colorectal, liver or gastric cancer. While pro-inflammatory cytokines within the tumor microenvironment probably contribute to FAT10 overexpression, an increasing body of evidence argues that pro-malignant capacities of FAT10 itself largely underlie its broad and intense overexpression in tumor tissues. FAT10 thereby regulates pathways involved in cancer development such as the NF-κB- or Wnt-signaling. Moreover, FAT10 directly interacts with and influences downstream targets such as MAD2, p53 or β-catenin, leading to enhanced survival, proliferation, invasion and metastasis formation of cancer cells but also of non-malignant cells. In this review we will provide an overview of the regulation of FAT10 expression as well as its function in carcinogenesis.