Loss of Runx3 Is a Key Event in Inducing Precancerous State of the Stomach

Ito, Kosei; Chuang, Linda Shyue Huey; Ito, Tomoko; Chang, Ti Ling; Fukamachi, Hiroshi; Salto–Tellez, Manuel; Ito, Yoshiaki

doi:10.1053/j.gastro.2011.01.043

Cited by 68 publications

(80 citation statements)

References 42 publications

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“…This transcription factor has been originally identified as a tumor suppressor, and RUNX3 loss is seen as an early event in gastric cancer development due to aberrant Wnt signaling, causing spontaneous epithelial-mesenchymal transition (EMT) and producing a tumorigenic stem cell-like subpopulation [126][127][128] . Furthermore, recent evidence suggests that RUNX3 can either suppress or activate Wnt signaling activity in gastric cancer by binding to the TCF4⁄b-catenin complex, depending of (or regulated by) cell context-dependent mechanisms [129] .…”

Section: Loss Of Wnt Repressor Function In Gastric Cancermentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

261

219

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Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput "omics" approaches will help in the search for Wnt pathway antagonist in the near future.

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Section: Loss Of Wnt Repressor Function In Gastric Cancermentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

261

219

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“…17 RUNX3, with its encoding gene located on chromosome 1p36, is involved in gastric epithelial growth 8,12 and T-cell differentiation. 18 Mislocalization of RUNX3 leading to its activation has been reported to result in a loss of nuclear RUNX3 expression in 44% of gastric carcinoma cases and cytoplasmic mislocalization in 38% of cases.…”

Section: Discussionmentioning

confidence: 99%

“…9 RUNX3 inactivation occurs early during the progression to malignancy. 10,12,13 In the current study, we investigated the association be- …”

Section: 나윤주 등 위암에서 Runx3 불활성화와 임상병리학적 특성과의 관계mentioning

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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“…Estudios previos demostraron, que la inactivación de RUNX3 desencadena un estado precanceroso en el intestino y epitelio gástrico de ratones, caracterizado por la pérdida de células epiteliales e inflamación; además de activar la vía Wnt e incrementar la expresión de genes blancos de esta (Ito et al 2005(Ito et al , 2011.…”

Section: Gen Runx3 (Runt-related Transcription Factor 3)unclassified

“…La inactivación del gen RUNX3 se relaciona de forma indirecta con esta sobreexpresión porque, normalmente, RUNX3 inhibe el complejo β-catenina/TCF4 y este complejo es el encargado de unirse al promotor de MYC y permitir la transcripción de este por la vía Wnt (Ito et al 2011). La sobreexpresión de MYC se asocia con tumores más agresivos, principalmente en CG-TI (Panani 2008) y con mal pronóstico (de Souza et al 2013, Nobili et al 2011, Panani y Roussos 2005.…”

Section: Gen Myc (V-myc Avian Myelocytomatosis Viral Oncogene Homolog)unclassified

Factores genéticos y epigenéticos del cáncer gástrico

2017

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ResumenEl cáncer gástrico (CG) es la primera causa de muerte por cáncer en Colombia, la tumorogénesis gástrica es un proceso gradual y de larga evolución que incluye cambios genéticos y epigenéticos que activan protooncogenes e inactivan genes supresores de tumor (GST). Los cambios genéticos incluyen pérdida de heterocigocidad (LOH), inestabilidad microsatelital (MSI), translocaciones, aneuploidía, y mutaciones en GST; y amplificaciones o mutaciones en protooncogenes. Por otro lado, la alteración epigenética más frecuente es la metilación de los promotores. En la actualidad, el CG es un problema de salud pública en Colombia por tres factores: las altas tasas de incidencia/mortalidad, los sobrecostos de los tratamientos de la enfermedad en estadios avanzado y la falta de acceso de la población a los servicios de salud. Esta revisión expondrá las alteraciones genéticas y epigenéticas que se encuentran con mayor frecuencia en CG, y su asociación con los diferentes tipos de CG.Palabras clave: cáncer gástrico, genes supresores de tumor, genética, metilación, oncogenes AbstractGastric cancer (GC) is the leading cause of cancer death in Colombia, gastric tumorigenesis is a gradual and long evolution process involving genetic and epigenetic changes that activate protooncogenes and inactivate tumor suppressor genes (GST). The genetic changes include loss of heterozygosity (LOH), microsatellite instability (MSI), translocations, aneuploidy, and mutations in GST; and mutations in protooncogenes or amplifications. Meanwhile, methylation of promoters is the commonest epigenetic alteration. Actually, CG is a public health problem in the country for three factors: high rates of incidence/mortality, overruns treatments for advanced disease stages and lack of public access to services health. This review the genetic and epigenetic alterations that are found more often in CG, and its association with different types of CG.

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Loss of Runx3 Is a Key Event in Inducing Precancerous State of the Stomach

Cited by 68 publications

References 42 publications

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

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

Factores genéticos y epigenéticos del cáncer gástrico

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