FAT10 level in human gastric cancer and its relation with mutant p53 level, lymph node metastasis and TNM staging

Ji, Feng; Jin, Xi; Jiao, Chunhua; Xu, Qinwei; Wang, Ziwei; Chen, Yueliang

doi:10.3748/wjg.15.2228

Cited by 38 publications

(41 citation statements)

References 16 publications

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“…These data imply that mutant p53, as found in many tumors, would elevate FAT10 expression and along with it FAT10's pro-malignant capacities . In support of this hypothesis, the mRNA and protein expression levels of FAT10 positively correlated with the mRNA and protein expression levels of mutant p53 in gastric cancer tissue and patients with high FAT10 expression in their tumors showed a tendency towards unfavorable prognosis regarding the overall survival rate (Ji et al, 2009).…”

Section: P53mentioning

confidence: 60%

“…Moreover, in several cancer types a statistically significant association between a high FAT10 expression level and the progression and severity of the disease including a higher propensity for metastasis formation and poor prognosis, has been reported. These include triple-negative breast cancer (Han et al, 2015), glioma (Dai et al, 2016;Yuan et al, 2012), pancreatic ductal adenocarcinoma , HCC , or gastric cancer (Ji et al, 2009). Furthermore, colon cancer patients treated with a postoperative chemotherapy and bearing tumors with high FAT10 expression displayed a higher recurrence rate than those with FAT10-negative tumors and FAT10 expression was associated with a significantly shorter survival time (Zhao et al, 2015).…”

Section: Fat10 Expression Levels In Different Cancer Typesmentioning

confidence: 99%

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The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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a b s t r a c tDuring 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-␥ and TNF-␣ 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-B-or Wnt-signaling. Moreover, FAT10 directly interacts with and influences downstream targets such as MAD2, p53 or ␤-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.

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Section: P53mentioning

confidence: 60%

Section: Fat10 Expression Levels In Different Cancer Typesmentioning

confidence: 99%

The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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“…Recently, there have been an increasing number of studies on FAT10 in malignant tumors. The FAT10 gene is overexpressed in various cancers, such as gastrointestinal cancer, HCC, pancreatic ductal adenocarcinoma, and human glioma (8)(9)(10)(11)(12). In the liver, FAT10 overexpression is an epigenetic marker for liver neoplasia (13).…”

Section: Introductionmentioning

confidence: 99%

Ubiquitin-like Protein FAT10 Promotes the Invasion and Metastasis of Hepatocellular Carcinoma by Modifying β-Catenin Degradation

et al. 2014

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The ubiquitin-like protein FAT10 and the homeobox protein HOXB9 each promote metastatic progression in hepatocellular carcinoma (HCC). In this study, we investigated the clinicopathologic significance of FAT10 and HOXB9 in HCC and investigated a mechanistic role for FAT10 in HOXB9-mediated invasiveness and metastasis. Relative to adjacent normal tissues, FAT10 and HOXB9 were markedly overexpressed in HCC, where a positive correlation in their expression and associated malignant characteristics were found. RNAi-mediated silencing of FAT10 decreased HOXB9 expression and inhibited HCC invasion and metastasis in vitro and in vivo. The effects of FAT10 silencing were reversed by HOXB9 overexpression, whereas RNAi-mediated silencing of HOXB9 decreased HCC invasion and metastasis driven by FAT10 overexpression. Mechanistically, FAT10 regulated HOXB9 expression by modulating the b-catenin/TCF4 pathway, directly binding to b-catenin and preventing its ubiquitination and degradation. Together, our results identified a novel HCC regulatory circuit involving FAT10, b-catenin/TCF4, and HOXB9, the dysfunction of which drives invasive and metastatic character in HCC.

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“…Significantly, FAT10 was found to be highly upregulated in the tumors of hepatocellular carcinoma (HCC) and other gastrointestinal cancers (Ji et al, 2009;Lee et al, 2003;Lukasiak et al, 2008), non-small cell lung cancer (Heighway et al, 2002) as well as mantle cell lymphoma (Martinez et al, 2003). FAT10 was even recently implicated to be a HCC stemcell marker (Oliva et al, 2010b) as well as an epigenetic marker for liver preneoplasia in a drug-primed mouse model of tumorigenesis (Oliva et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

FAT10 mediates the effect of TNF-α in inducing chromosomal instability

Ren

Wang

Gao

et al. 2011

Journal of Cell Science

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SummaryTumor necrosis factor-alpha (TNF-a) plays important roles in chronic inflammation-associated tumorigenesis but the mechanisms involved remain poorly understood. Previously, we reported that high levels of FAT10 led to chromosomal instability that is mediated by an abbreviated mitotic phase. Here, we show that TNF-a induces FAT10 gene expression through TNF receptor 1 (TNFR1) and activates the NF-kB pathway in HCT116 and SW620 cells. TNF-a treatment also leads to an abbreviated mitotic phase that can be reversed by inhibiting FAT10 expression. This abbreviated mitotic phase is correlated with a TNF-a-induced reduction in the kinetochore localization of MAD2 during prometaphase which, again, can be reversed by inhibiting FAT10 gene expression. There is greater variability of chromosome numbers in HCT116 and SW620 cells treated with TNF-a than in untreated cells, which can be reversed by the introduction of short hairpin RNA (shRNA) against FAT10. The more stable chromosome numbers in HCT116 cells expressing FAT10 shRNA can revert to greater variability with the addition of a mutant FAT10 that is not recognized by the FAT10 shRNA. Upon TNF-a stimulation, higher cell death is observed when FAT10 expression is inhibited by shRNA. These data strongly suggest that FAT10 plays an important role in mediating the function of TNF-a during tumorigenesis by inducing cell cycle deregulation and chromosomal instability, and by inhibiting apoptosis.

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FAT10 level in human gastric cancer and its relation with mutant p53 level, lymph node metastasis and TNM staging

Abstract: FAT10 may be involved in gastric carcinogenesis, and is a potential marker for the prognosis of gastric cancer patients. FAT10 and mutant p53 may play a common role in the carcinogenesis of gastric cancer.

Cited by 38 publications

References 16 publications

The ubiquitin-like modifier FAT10 in cancer development

The ubiquitin-like modifier FAT10 in cancer development

Ubiquitin-like Protein FAT10 Promotes the Invasion and Metastasis of Hepatocellular Carcinoma by Modifying β-Catenin Degradation

FAT10 mediates the effect of TNF-α in inducing chromosomal instability

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