Protein tyrosine kinase 7: a hepatocellular carcinoma-related gene detected by triple-combination array

Hishida, Mitsuhiro; Inokawa, Yoshikuni; Takano, Nao; Nishikawa, Yoko; Iwata, Nakao; Kanda, Mitsuro; Tanaka, Chie; Kobayashi, Daisuke; Yamada, Suguru; Nakayama, Goro; Fujii, Tsutomu; Sugimoto, Hiroyuki; Koike, Masahiko; Fujiwara, Michitaka; Kodera, Yasuhiro; Nomoto, Shuji

doi:10.1016/j.jss.2014.12.045

Cited by 10 publications

(9 citation statements)

References 40 publications

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“…SRD5A2 (steroid 5 alpha-reductase 2) is an androgen metabolic gene linked to prostrate and breast cancer and shown to undergo age-dependent hypermethylation and downregulation of expression (Ge et al, 2015; Hein et al, 2012). PTK7 (protein tyrosine kinase 7) plays a role in the Wnt signaling pathway and linked to several different cancers and reported to undergo hypermethylation in hepatic cancer cells (Dunn and Tolwinski, 2016; Hishida et al, 2015). SND1 (staphylococcal nuclease and tudor domain containing 1), a transcriptional co-activator, is implicated in different cancers and methylation status of this gene is considered as a potential biomarker of colorectal cancer (Naumov et al, 2013; Navarro-Imaz et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Conserved effect of aging on DNA methylation and association with EZH2 polycomb protein in mice and humans

Mozhui

Pandey

2017

Mechanisms of Ageing and Development

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In humans, DNA methylation at specific CpG sites can be used to estimate the ‘epigenetic clock’, a biomarker of aging and health. The mechanisms that regulate the aging epigenome and level of conservation are not entirely clear. We performed affinity-based enrichment with methyl-CpG binding domain protein followed by high-throughput sequencing (MBD-seq) to assay DNA methylation in mouse samples. Consistent with previous reports, aging is associated with increase in methylation at CpG islands that likely overlap regulatory regions of genes that have been implicated in cancers (e.g., C1ql3, Srd5a2 and Ptk7). The differentially methylated regions in mice have high sequence conservation in humans and the pattern of methylation is also largely conserved between the two species. Based on human ENCODE data, these sites are targeted by polycomb proteins, including EZH2. Chromatin immunoprecipitation confirmed that these regions interact with EZH2 in mice as well, and there may be reduction in EZH2 occupancy with age at C1ql3. This adds to the growing evidence that EZH2 is part of the protein machinery that shapes the aging epigenome. The conservation in both sequence and methylation patterns of the age-dependent CpGs indicate that the epigenetic clock is a fundamental feature of aging in mammals.

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Section: Discussionmentioning

confidence: 99%

Conserved effect of aging on DNA methylation and association with EZH2 polycomb protein in mice and humans

Mozhui

Pandey

2017

Mechanisms of Ageing and Development

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“…We identified several genes as candidates for TSGs in HCC using this combination array analysis. we listed these putative TSGs detected by combination array analysis in Table III (100)(101)(102)(103)(104)(105)(106)(107)(108)(109)(110)(111)(112).…”

Section: Tsgs In Hccmentioning

confidence: 99%

Search for useful biomarkers in hepatocellular carcinoma, tumor factors and background liver factors

et al. 2017

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Hepatocarcinogenesis is a complex and multistep process that involves the accumulation of genetic and epigenetic alterations in regulatory genes. To understand the development of hepatocellular carcinoma (HCC), current research has utilized improved array technologies. The identification of cancer-related molecules could lead to the development of novel molecular targets for treatment and biomarkers for predicting prognosis. However, prognostic prediction is insufficient when considering only tumor factors, since hepatocarcinogenesis is also greatly influenced by the status of the background liver. Clinical background liver factors, such as the presence of chronic active hepatitis or cirrhosis, are well known as risk factors for developing HCC. In contrast, genetic or epigenetic background liver factors remain unknown, albeit those are important to understand the developing process of HCC. Investigating background liver factors could contribute to the development of carcinogenic markers of HCC and to the prevention of the development of HCC. In the present study, we review the currently identified tumor factors and background liver factors from a molecular biological viewpoint and also introduce our combination array analysis.

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“…Wong et al (81) detected the downregulation of miRNA-223 expression levels in HCC tissues and investigated stathmin 1 (STMN1) as a downstream target. Methylation array analysis has been used to detect cancer-specific epigenetic alterations in HCC (82)(83)(84)(85)(86)(87)(88)(89)(90)(91). Shen et al (82) analyzed tumor and adjacent non-tumor tissue samples from 62 Taiwanese patients with HCC, using Illumina ® methylation arrays, and identified several genes that were hyper-or hypo-methylated in tumor tissues, as compared with adjacent non-tumor tissues (82).…”

Section: Molecular Alterations In Hcc Tumorsmentioning

confidence: 99%

“…The candidate genes were pyrosequenced and the array data was validated; analysis of plasma DNA suggested those genes may be used as biomarkers for early-stage HCC. Okamura et al (83) created a triple-combination array, consisting of an SNP array, gene expression microarray and methylation array analysis (83)(84)(85)(86)(87)(88)(89). The tumor-suppressor gene candidates were efficiently identified by detecting downregulation and methylation in tumor tissues, and without chromosomal deletion of the loci of the targeted genes.…”

Section: Molecular Alterations In Hcc Tumorsmentioning

confidence: 99%

Molecular alterations in the carcinogenesis and progression of hepatocellular carcinoma: Tumor factors and background liver factors

et al. 2016

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Abstract. Although hepatocellular carcinoma (HCC) is associated with poor prognosis worldwide, the molecular mechanisms underlying the carcinogenesis and progression of this disease remain unclear. Several tumor characteristics have previously been demonstrated to be prognostic factors of survival following hepatic resection, or the recurrence of HCC or other types of cancer. Comparisons of normal tissues and HCC tumor tissues have revealed the presence of numerous molecular alterations in HCC, including genetic and epigenetic mechanisms, particularly mutations in certain genes and DNA methylation in the promoter regions of tumor-suppressor genes. A number of studies have previously used array analysis to detect variations in the expression levels of cancer-associated genes and microRNAs, and in DNA methylation. However, an investigation of HCC tumor tissues may not determine the effect of noncancerous liver tissues (background liver) in patients with HCC. As HCC may recur multicentrically following resection, a damaged or chronically diseased HCC background liver may be considered as a pre-cancerous organ. Therefore, the influence of the background liver on HCC requires further study. Detailed studies regarding the background liver may be essential for the improved understanding of the carcinogenesis and progression of this malignancy; however only a few studies have investigated the microenvironment of the HCC background liver. The present review discusses prior molecular studies of hepatocarcinogenesis that focus on HCC and background liver tissues.

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Protein tyrosine kinase 7: a hepatocellular carcinoma-related gene detected by triple-combination array

Cited by 10 publications

References 40 publications

Conserved effect of aging on DNA methylation and association with EZH2 polycomb protein in mice and humans

Conserved effect of aging on DNA methylation and association with EZH2 polycomb protein in mice and humans

Search for useful biomarkers in hepatocellular carcinoma, tumor factors and background liver factors

Molecular alterations in the carcinogenesis and progression of hepatocellular carcinoma: Tumor factors and background liver factors

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