Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Song, Hyun Joo; Shim, Ki–Nam; Joo, Yang-Hee; Kim, Seong‐Eun; Jung, Sung-Ae; Yoo, Kwon

doi:10.5009/gnl.2008.2.2.119

Cited by 11 publications

(8 citation statements)

References 26 publications

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“…Hence, RUNX3 P2 hypermethylation in cancer is not associated with its silencing. Of note, RUNX3 P2 methylation in GC was found to be mostly monoallelic [88], so even if methylation completely silenced the expression of just one allele, the remaining allele could still be functional and express RUNX3. As mentioned earlier, RUNX3 expression is regulated by two promoters.…”

Section: Runx3 Promoter Hypermethylation Is Not a Driver Of Gc Or Othmentioning

confidence: 99%

Runx3 at the interface of immunity, inflammation and cancer

Lotem

Levanon

Negreanu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Inactivation of tumor suppressor genes (TSG) in normal cells provides a viability/growth advantage that contributes cell-autonomously to cancer. More than a decade ago claims arose that the RUNX3 member of the RUNX transcription factor family is a major TSG inactivated in gastric cancer, a postulate extended later to other cancers. However, evidence that Runx3 is not expressed in normal gastric and other epithelia has challenged the RUNX3-TSG paradigm. Here we critically re-appraise this paradigm in light of recent high-throughput, quantitative genome-wide studies on thousands of human samples of various tumors and new investigations of the role of Runx3 in mouse cancer models. Collectively, these studies unequivocally demonstrate that RUNX3 is not a bona fide cell-autonomous TSG. Accordingly, RUNX3 is not recognized as a TSG and is not included among the 2000 cancer genes listed in the "Cancer Gene Census" or "Network for Cancer Genes" repositories. In contrast, RUNX3 does play important functions in immunity and inflammation and may thereby indirectly influence epithelial tumor development.

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Section: Runx3 Promoter Hypermethylation Is Not a Driver Of Gc Or Othmentioning

confidence: 99%

Runx3 at the interface of immunity, inflammation and cancer

Lotem

Levanon

Negreanu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…Hot FIREPol DNA Polymerase from Solis BioDyne (Tartu, Estonia) was used in all the reactions. The primers and reaction conditions for MSP were chosen based on previously published data (17)(18)(19)(20)(21). All the primers were obtained from Oligo.pl (Warsaw, Poland).…”

Section: Methylation-specific Pcrmentioning

confidence: 99%

Frequent hypermethylation of WNT pathway genes in laryngeal squamous cell carcinomas

Paluszczak

Hemmerling

Kostrzewska-Poczekaj

et al. 2014

J Oral Pathology Medicine

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“…9 Inactivation of RUNX3 by promoter methylation was reported in 45-65% of all gastric carcinomas. 10,19,20 Most reported cases of gastric carcinoma in East Asia are associated with CagA-positive H. pylori infection. In comparison to the Western CagA-positive H. pylori strain, CagA in East Asia more often causes severe gastric mucosal inflammation and is associated with severe atrophic gastritis and gastric adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

RUNX3Methylation, Loss of RUNX3 Expression and Clinicopathologic Findings according toHelicobacter pyloriCagA in Gastric Carcinoma

Shim

Joo

et al. 2015

Korean J Gastroenterol

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Background/Aims: Helicobacter pylori cytotoxin-associated gene A (CagA) has been suggested to be involved in the inactivation of Runt-related transcription factor 3 (RUNX3), a known gastric carcinoma tumor suppressor gene. It remains unclear how H. pylori CagA initiates or maintains RUNX3 promoter methylation and inactivates its protein expression in gastric carcinoma. Methods: RUNX3 promoter methylation status, RUNX3 expression, and H. pylori CagA were investigated in 76 sample pairs of gastric carcinoma tissue. The patients' medical records were reviewed. The association between RUNX3 methylation or loss of RUNX3 expression and clinicopathologic variables according to H. pylori CagA status were investigated. Results: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation did not show association with lymphatic invasion, venous invasion, and TNM stages. However RUNX3 methylation was observed more frequently in poorly differentiated adenocarcinoma and signet ring cell carcinoma (77.8% vs. 20.0%, p=0.023) in early stage. In gastric carcinoma patients with H. pylori CagA-positive infection, loss of RUNX3 expression did not show association with lymphatic invasion, venous invasion, and TNM stages. However loss of RUNX3 expression was observed more frequently in early gastric carcinoma than in advanced gastric carcinoma (84.2% vs. 75.0%, p=0.51), but this difference was not significant. Conclusions: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation or loss of RUNX3 expression did not show correlation with lymphovascular invasion and TNM stages. In early gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation was observed more in poorly differentiated adenocarcinoma and signet ring cell carcinoma. (Korean J Gastroenterol 2015;66:75-84)

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Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma

Cited by 11 publications

References 26 publications

Runx3 at the interface of immunity, inflammation and cancer

Runx3 at the interface of immunity, inflammation and cancer

Frequent hypermethylation of WNT pathway genes in laryngeal squamous cell carcinomas

RUNX3Methylation, Loss of RUNX3 Expression and Clinicopathologic Findings according toHelicobacter pyloriCagA in Gastric Carcinoma

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