Methylation Profiles of CpG Island Loci in Major Types of Human Cancers

Park, Seog-Yun; Kim, Baek-Hee; Kim, Jeong-Ho; Cho, Nam-Yun; Choi, Minhee; Yu, Eun Joo; Lee, Sun; Kang, Gyeong Hoon

doi:10.3346/jkms.2007.22.2.311

Cited by 25 publications

(16 citation statements)

References 30 publications

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“…11 However, the role of RUNX3 as a possible gastric tumor suppressor is yet controversial. 7,12,[14][15][16] Moreover, the results of present study are not consistent with those of the previous reports in that the positive MSP expression of the RUNX3 gene was found only in 32.9% of the patients, which is relatively lower than those of the previous reports (45-69%), 7,8 including the Korean-specific data (56-64%).…”

Section: Discussionmentioning

confidence: 99%

“…12 In addition, methylation of the multiple tumor suppressor genes including RUNX3 were found to increase with age in the nonneoplastic gastric epithelia. 13 Although the absence of RUNX3 expression has been reported in several studies on the human gastric carcinoma, 7,11,12,14,15 a recent study reported that the immunohistochemical staining detected the RUNX3 protein expression in the infiltrating leukocytes, but not in the gastric epithelium. 16 Therefore, the low levels of RUNX3 expression in the gastric epithelium and the absence of downregulation of RUNX3 in the gastric cancer do not support the idea that RUNX3 functions as a gastric tumor suppressor gene.…”

Section: Introductionmentioning

confidence: 99%

“…10 Methylation of RUNX3 is frequently found in major types of the human cancers. 11 These types include gastric cancer (64%), hepatocellular carcinoma (73%), lung cancer (46%), breast cancer (25%), and colon cancer (4.9%). 12 However, RUNX3 methylation has also been found in the nonneo-plastic tissues including the premalignant lesions of gastric carcinoma such as chronic gastritis (8.1%), intestinal metaplasia (28.1%), and gastric adenoma (27.3%).…”

Section: Introductionmentioning

confidence: 99%

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Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Song

Shim²,

Joo³

et al. 2008

Gut Liver

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Background/Aims: RUNX3 (PEBP2αC/CBFA3/AML2) is a novel tumor suppressor gene in the human gastric carcinoma. The aims of this study were to determine the methylation of RUNX3 promoter and the association between RUNX3 methylation and the clinicopathological characteristics of patients with gastric carcinoma. Methods: Seventy-nine patients with gastric carcinoma were studied prospectively from April 2005 to May 2007. The methylations of RUNX3 promoter on the gastric carcinoma specimens and the corresponding nonneoplastic mucosa were evaluated by methylation-specific polymerase chain reaction. Results: Comparison of the results with the clinicopathological characteristics identified RUNX3 monoallelic methylation in 32.9% (26/79) of the gastric carcinoma patients and in 11.4% (9/79) of those with nonneoplastic mucosa (p=0.053). The monoallelic methylated gastric carcinoma specimens predominantly consisted of well-and moderately differentiated carcinomas (44.7%), with the unmethylated group constituting 22.0% of them (p=0.031). Among the 48 patients (60.8%) who underwent gastrectomy, there was no correlation between the two groups with regard to Lauren's classification (p=0.235), depth of invasion (p=0.990), nodal status (p=0.601), stage (p=0.900), lymphatic invasion (p=0.537), and vascular invasion (p=0.815). Conclusions: Methylation of the tumor suppressor gene RUNX3 might be one of the mechanisms involved in the pathogenesis of gastric carcinoma. (Gut and Liver 2008;2:119-125)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Song

Shim²,

Joo³

et al. 2008

Gut Liver

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“…DNA methylation is the most common and important mechanism of TSGs inactivation in various human carcinoma (Grønbaek et al, 2007;Dachrut et al, 2009). It's worth noting that hypermethylation of TSGs may occur in early stage of carcinogeneses of dysplasia cells (Park et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Alteration of Runt-related Transcription Factor 3 Gene Expression and Biologic Behavior of Esophageal Carcinoma TE-1 Cells after 5-Azacytidine Intervention

Wang

Liu²,

Akhtar³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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5-Azacytidine (5-azaC) was originally identified as an anticancer drug (NSC102876) which can cause hypomethylation of tumor suppressor genes. To assess its effects on runt-related transcription factor 3 (RUNX3), expression levels and the promoter methylation status of the RUNX3 gene were assessed. We also investigated alteration of biologic behavior of esophageal carcinoma TE-1 cells. MTT assays showed 5-azaC inhibited the proliferation of TE-1 cells in a time and dose-dependent way. Although other genes could be demethylated after 5-azaC intervention, we focused on RUNX3 gene in this study. The expression level of RUNX3 mRNA increased significantly in TE-1 cells after treatment with 5-azaC at hypotoxic levels. RT-PCR showed 5-azaC at 50 µM had the highest RUNX3-induction activity. Methylation-specific PCR indicated that 5-azaC induced RUNX3 expression through demethylation. Migration and invasion of TE-1 cells were inhibited by 5-azaC, along with growth of Eca109 xenografts in nude mice. In conclusion, we demonstrate that the RUNX3 gene can be reactivated by the demethylation reagent 5-azaC, which inhibits the proliferation, migration and invasion of esophageal carcinoma TE-1 cells.

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“…[11][12][13] CpG methylation has recently been shown to be an important mechanism in the transcriptional inactivation of E-cadherin, and CpG methylation around the promoter region of E-cadherin was found to be significantly correlated with reduced E-cadherin expression in various cancers. 14 Though it has been thought that hypermethylation of the E-cadherin gene is associated with immunohistochemical expression, tumor progression, tumor grade, tumor invasion, and lymph node metastasis in various tumors, this has been rarely studied in endometrial carcinoma of Korean women. In the current study, we analyzed methylation status of the E-cadherin and E-cadherin expression in endometrial hyperplasias and endometrial carcinomas.…”

Section: Introductionmentioning

confidence: 99%

Hypermethylation of E-cadherin in endometrial carcinoma

et al. 2008

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Objective: Hypermethylation of CpG island is a common mechanism for the inactivation of tumor suppressor genes. Hypermethylation of the E-cadherin promoter region has been rarely studied in endometrial carcinoma of Korean women. The purpose of this study is to investigate methylation status of E-cadherin promoter region in endometrial carcinomas and endometrial hyperplasias, and analyze the correlation with clinicopathologic variables in endometrial carcinomas. Methods: We examined the methylation status of the E-cadherin promoter region using methylation specific polymerase chain reaction and immunohistochemical expression (IHC) of E-cadherin in 30 endometrioid endometrial carcinomas and 20 endometrial hyperplasias, and correlated these results with various clinicopathological factors of endometrial carcinomas. Results: Decreased expression of E-cadherin was detected in 13 of 30 (43.3%) endometrial carcinomas and in 1 of 20 (5%) endometrial hyperplasias (p=0.009). Promoter hypermethylation was detected in 12 of 30 (40%) endometrial carcinomas and 2 of 20 (10%) endometrial hyperplasias (p=0.015). Methylation status did not have a significant influence on the tumor grade and lymph node metastasis. However, the hypermethylation rate was significantly higher in stage above Ic (p=0.025). Decreased expression of E-cadherin was associated with tumor grade, tumor stage, and lymph node metastasis in endometrial carcinomas (p=0.01, p=0.02, p=0.03). There was no correlation between DNA hypermethylation and decreased expression of E-cadherin in endometrial carcinomas (p＞0.05). Conclusion:These results indicate that hypermethylation of E-cadherin promoter region is a frequent event in endometrial carcinoma, which may play an important role in the progression of carcinogenesis. Also, the promoter methylation of E-cadherin in endometrial carcinoma was found to be significantly associated with higher stage above Ic.

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Methylation Profiles of CpG Island Loci in Major Types of Human Cancers

Cited by 25 publications

References 30 publications

Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Alteration of Runt-related Transcription Factor 3 Gene Expression and Biologic Behavior of Esophageal Carcinoma TE-1 Cells after 5-Azacytidine Intervention

Hypermethylation of E-cadherin in endometrial carcinoma

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