LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma

Huang, Guo Liang; Li, Bin Kui; Zhang, Mei Yin; Zhang, Hui Zhong; Wei, Rong; Yuan, Yunfei; Shi, Ming; Chen, Xiao Qian; Huang, Long; Li, An Hua; Huang, Bi; Li, Hong Hua; Wang, Hui Yun

doi:10.3748/wjg.v16.i16.2046

Cited by 13 publications

(13 citation statements)

References 35 publications

(38 reference statements)

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“…28 The loss of heterozygosity in NAA11 was shown to correlate with a poor prognosis in hepatocellular carcinoma patients. 29 Other than these, the biological functions of mNaa11p and hNaa11p are not known. The presence of two similar NatA complexes sharing the same ribosome docking subunit, but different catalytic subunits in the same human cells, 28 may imply a complementary role in regulating similar biological processes.…”

Section: Resultsmentioning

confidence: 99%

Expression of humanNAA11(ARD1B) gene is tissue-specific and is regulated by DNA methylation

et al. 2011

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Section: Resultsmentioning

confidence: 99%

Expression of humanNAA11(ARD1B) gene is tissue-specific and is regulated by DNA methylation

et al. 2011

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“…For example, LOH in the genes ARD1 homolog B ( S. cerevisiae ) ( ARD1B ) and Mus musculus septin 11 ( SEPT11 ) were found to be significant prognostic factors for poor OS[63], and LOH in mannose 6-phosphate/insulin-like growth factor 2 receptor ( M6P/IGF2R ) was found to be predictive of poor clinical outcomes in surgically resected primary HCC patients[64]. …”

Section: Genomic Instabilitymentioning

confidence: 99%

“…However, there are still many important LOH regions that must be explored with regard to the genes that are involved in carcinogenesis and their biological and clinical implications[63]. …”

Section: Genomic Instabilitymentioning

confidence: 99%

Genetic alterations in hepatocellular carcinoma: An update

Niu¹,

Niu²,

Wang³

2016

WJG

137

108

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Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Although recent advances in therapeutic approaches for treating HCC have improved the prognoses of patients with HCC, this cancer is still associated with a poor survival rate mainly due to late diagnosis. Therefore, a diagnosis must be made sufficiently early to perform curative and effective treatments. There is a need for a deeper understanding of the molecular mechanisms underlying the initiation and progression of HCC because these mechanisms are critical for making early diagnoses and developing novel therapeutic strategies. Over the past decade, much progress has been made in elucidating the molecular mechanisms underlying hepatocarcinogenesis. In particular, recent advances in next-generation sequencing technologies have revealed numerous genetic alterations, including recurrently mutated genes and dysregulated signaling pathways in HCC. A better understanding of the genetic alterations in HCC could contribute to identifying potential driver mutations and discovering novel therapeutic targets in the future. In this article, we summarize the current advances in research on the genetic alterations, including genomic instability, single-nucleotide polymorphisms, somatic mutations and deregulated signaling pathways, implicated in the initiation and progression of HCC. We also attempt to elucidate some of the genetic mechanisms that contribute to making early diagnoses of and developing molecularly targeted therapies for HCC.

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“…This inactivation of the NAA11 allele was shown to correlate to a low survival rate. 82 A complete overview of the current knowledge of the expression patterns of hNaa10p, hNaa11p and hNaa15p is given in Table 1.…”

Section: The Role and Expression Of Other Nata Subunits In Cancer Cellsmentioning

confidence: 99%

Protein N-terminal acetyltransferases in cancer

2012

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The human N-terminal acetyltransferases (NATs) catalyze the transfer of acetyl moieties to the N-termini of 80-90% of all human proteins. Six NAT types are present in humans, NatA-NatF, each is composed of specific subunits and each acetylates a set of substrates defined by the N-terminal amino-acid sequence. NATs have been suggested to act as oncoproteins as well as tumor suppressors in human cancers, and NAT expression may be both elevated and decreased in cancer versus non-cancer tissues. Manipulation of NATs in cancer cells induced cell-cycle arrest, apoptosis or autophagy, implying that these enzymes target a variety of pathways. Of particular interest is hNaa10p (human ARD1), the catalytic subunit of the NatA complex, which was coupled to a number of signaling molecules including hypoxia inducible factor-1α, β-catenin/cyclin D1, TSC2/mammalian target of rapamycin, myosin light chain kinase , DNA methyltransferase1/E-cadherin and p21-activated kinase-interacting exchange factors (PIX)/Cdc42/Rac1. The variety of mechanistic links where hNaa10p acts as a NAT, a lysine acetyltransferase or displaying a non-catalytic role, provide insights to how hNaa10p may act as both a tumor suppressor and oncoprotein.

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LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma

Cited by 13 publications

References 35 publications

Expression of humanNAA11(ARD1B) gene is tissue-specific and is regulated by DNA methylation

Expression of humanNAA11(ARD1B) gene is tissue-specific and is regulated by DNA methylation

Genetic alterations in hepatocellular carcinoma: An update

Protein N-terminal acetyltransferases in cancer

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