Promoter hypermethylation ofCDH1,FHIT,MTAPandPLAGL1in gastric adenocarcinoma in individuals from Northern Brazil

Leal, Mariana Ferreira; Lima, Eleonidas Moura; Silva, Patrícia Natália Oliveira da; Assumpção, Paulo Pimentel de; Calcagno, Danielle Queiroz; Payão, Spencer Luíz Marques; Burbano, Rommel Rodrı́guez; Smith, Marília de Arruda Cardoso

doi:10.3748/wjg.v13.i18.2568

Cited by 45 publications

(28 citation statements)

References 42 publications

(34 reference statements)

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“…In this paper, we used this approach to identify genes that are differentially methylated in gastric cancer cell lines versus normal stomach tissue. Several TSGs previously identified as being regulated by DNA methylation in gastric cancer, including CDH13 (Hibi et al, 2004), FHIT (Leal et al, 2007), KLK10 (Huang et al, 2007), hMLH1 (Kim et al, 2003a;Brucher et al, 2006;Sato and Meltzer, 2006), HRK (Obata et al, 2003), DLC1 (Kim et al, 2003c;Liao and Lo, 2008), and PLAU (Yamashita et al, 2006), were also identified by our CpG microarray system (data not shown). In addition to LRP1B as a potential gastric cancer tumor suppressor subject to regulation by DNA methylation, we also identified Glutamate receptor, ionotropic, kainite 2 (GRIK2) as another novel candidate TSG in gastric cancer (Wu et al, 2009).…”

Section: Discussionsupporting

confidence: 54%

Aberrant methylation impairs low density lipoprotein receptor‐related protein 1B tumor suppressor function in gastric cancer

Lu¹,

et al. 2010

Genes Chromosomes & Cancer

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DNA methylation plays a significant role in tumor progression. In this study, we used CpG microarray and differential methylation hybridization approaches to identify low density lipoprotein receptor-related protein 1B (LRP1B) as a novel epigenetic target in gastric cancer. LRP1B was hypermethylated in four gastric cancer cell lines, and low LRP1B mRNA expression was associated with high methylation levels in gastric cancer cell lines. Addition of a DNA methylation inhibitor (5-Aza-dC) restored the mRNA expression of LRP1B in these cell lines, indicating that DNA methylation is involved in regulating LRP1B expression. In 45 out of 74 (61%) clinical samples, LRP1B was highly methylated; LRP1B mRNA expression was significantly lower in 15 out of 19 (79%, P < 0.001) gastric tumor tissues than in corresponding adjacent normal tissues. In addition, ectopic expression of mLRP1B4 in gastric cancer cell lines suppressed cell growth, colony formation and tumor formation in nude mice. These results collectively indicate that LRP1B is a functional tumor suppressor gene in gastric cancer and that is regulated by DNA methylation.

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Section: Discussionsupporting

confidence: 54%

Aberrant methylation impairs low density lipoprotein receptor‐related protein 1B tumor suppressor function in gastric cancer

Lu¹,

et al. 2010

Genes Chromosomes & Cancer

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“…This observation may be due to the increased CpG island methylation related in stomach [26]. In our population, we previously detected DNA promoter methylation of other tumor suppressor genes in normal gastric mucosa [27,28]. This gene may be commonly methylated in the stomachs of individual from Northern Brazil.…”

Section: Discussionmentioning

confidence: 56%

Insulin-like growth factor binding protein-3 gene methylation and protein expression in gastric adenocarcinoma

Gigek

Leal

Lisboa

et al. 2010

Growth Hormone & IGF Research

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“…FHIT may induce apoptosis by up-regulating Bak (Sard et al 1999). Hypermethylation in the promoter region of FHIT has been reported in a wide variety of cancers (Kim et al 2004a, Hong et al 2005, Goldberg et al 2006, Leal et al 2007. FHIT methylation in prostate cancer has only been described in one report, at a low frequency of 15% (Maruyama et al 2002).…”

Section: Fragile Histidine Triad (Fhit)mentioning

confidence: 99%

The emergence of DNA methylation as a key modulator of aberrant cell death in prostate cancer

Murphy

Perry²,

Lawler

2008

Endocrine Related Cancer

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It is now well established that cancer cells exhibit a number of genetic defects in the machinery that governs programmed cell death and that sabotage of apoptosis is one of the principal factors aiding in the evolution of the carcinogenic phenotype. A number of studies have implicated aberrant DNA methylation as a key survival mechanism in cancer, whereby promoter hypermethylation silences genes essential for many processes including apoptosis. To date, studies on the methylation profile of apoptotic genes have largely focused on cancers of the breast, colon and stomach, with only limited data available on prostate cancer. Here we discuss the major developments in the field of DNA methylation and its role in the regulation of aberrant apoptosis in prostate cancer. The most significant advances have involved the discovery of apoptotic gene targets of methylation, including XAF1, (fragile histidine triad (FHIT ), cellular retinol binding protein 1 (CRBP1), decoy receptor 1(DCR1), decoy receptor 2 (DCR2 ), target of methylation-induced silenceing 1 (TMS1), TNF receptor superfamily, member 6 (FAS), Reprimo (RPRM) and GLI pathogenesis-related 1 (GLIPR1). These genes are reported to be hypermethylated in prostate cancer and some offer potential as diagnostic and prognostic markers. We also introduce the concept of an 'apoptotic methylation signature' for prostate cancer and evaluate its potential in a diagnostic, prognostic and therapeutic setting.

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Promoter hypermethylation ofCDH1,FHIT,MTAPandPLAGL1in gastric adenocarcinoma in individuals from Northern Brazil

Cited by 45 publications

References 42 publications

Aberrant methylation impairs low density lipoprotein receptor‐related protein 1B tumor suppressor function in gastric cancer

Aberrant methylation impairs low density lipoprotein receptor‐related protein 1B tumor suppressor function in gastric cancer

Insulin-like growth factor binding protein-3 gene methylation and protein expression in gastric adenocarcinoma

The emergence of DNA methylation as a key modulator of aberrant cell death in prostate cancer

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