Runx3 expression in gastrointestinal tract epithelium: resolving the controversy

Ito, Kenichi; Inoue, Ken‐ichiro; Sc, Bae; Ito, Yoichi

doi:10.1038/onc.2008.496

Cited by 27 publications

(27 citation statements)

References 29 publications

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“…We thus concluded that RUNX3 is a gastric tumor suppressor gene that controls the growth, apoptosis, and differentiation of gastric epithelial cells [17][18][19][20] . Recently, RUNX3…”

Section: Introductionmentioning

confidence: 82%

Claudin-1 Has Tumor Suppressive Activity and Is a Direct Target of RUNX3 in Gastric Epithelial Cells

Chang

Ito

et al. 2010

Gastroenterology

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“…We thus concluded that RUNX3 is a gastric tumor suppressor gene that controls the growth, apoptosis, and differentiation of gastric epithelial cells [17][18][19][20] . Recently, RUNX3…”

Section: Introductionmentioning

confidence: 82%

Claudin-1 Has Tumor Suppressive Activity and Is a Direct Target of RUNX3 in Gastric Epithelial Cells

Chang

Ito

et al. 2010

Gastroenterology

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“…As the opposing viewpoints have already been discussed elsewhere, the reader is advised to refer to the respective publications (Bae and Ito, 2003;Levanon et al, 2003;Ito et al, 2009;Levanon and Groner, 2009). We anticipate that this controversy will soon be resolved with further in-depth studies.…”

Section: Controversy On Runx3 Expression In Gastrointestinal Tract Epmentioning

confidence: 98%

RUNX3 is multifunctional in carcinogenesis of multiple solid tumors

2010

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The study of RUNX3 in tumor pathogenesis is a rapidly expanding area of cancer research. Functional inactivation of RUNX3-through mutation, epigenetic silencing, or cytoplasmic mislocalization-is frequently observed in solid tumors of diverse origins. This alone indicates that RUNX3 inactivation is a major risk factor in tumorigenesis and that it occurs early during progression to malignancy. Conversely, RUNX3 has also been described to have an oncogenic function in a subset of tumors. Although the mechanism of how RUNX3 switches from tumor suppressive to oncogenic activity is unclear, this is of clinical relevance with implications for cancer detection and prognosis. Recent developments have significantly contributed to our understanding of the pleiotropic tumor suppressive properties of RUNX3 that regulate major signaling pathways. This review summarizes the important findings that link RUNX3 to tumor suppression.

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“…For example, Runx3-null balb/c mice can survive until adulthood , whereas FVB and C57BL/6 mice carrying the same Runx3 mutant allele die soon after birth (Ito et al, 2008). Differences in the gene targeting strategies could also explain the differences (Ito et al, 2009).…”

Section: Runx3 Insufficiency Leads To the Onset Of Lung Adenomas In Micementioning

confidence: 99%

Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer

Lee

et al. 2010

Oncogene

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Human lung adenocarcinoma, the most prevalent form of lung cancer, is characterized by many molecular abnormalities. K-ras mutations are associated with the initiation of lung adenocarcinomas, but K-ras-independent mechanisms may also initiate lung tumors. Here, we find that the runt-related transcription factor Runx3 is essential for normal murine lung development and is a tumor suppressor that prevents lung adenocarcinoma. Runx3À/À mice, which die soon after birth, exhibit alveolar hyperplasia. Importantly, Runx3À/À bronchioli exhibit impaired differentiation, as evidenced by the accumulation of epithelial cells containing specific markers for both alveolar (that is SP-B) and bronchiolar (that is CC10) lineages. Runx3À/À epithelial cells also express Bmi1, which supports self-renewal of stem cells. Lung adenomas spontaneously develop in aging Runx3 þ /À mice (B18 months after birth) and invariably exhibit reduced levels of Runx3. As K-ras mutations are very rare in these adenomas, Runx3 þ /À mice provide an animal model for lung tumorigenesis that recapitulates the preneoplastic stage of human lung adenocarcinoma development, which is independent of K-Ras mutation. We conclude that Runx3 is essential for lung epithelial cell differentiation, and that downregulation of Runx3 is causally linked to the preneoplastic stage of lung adenocarcinoma.

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Runx3 expression in gastrointestinal tract epithelium: resolving the controversy

Cited by 27 publications

References 29 publications

Claudin-1 Has Tumor Suppressive Activity and Is a Direct Target of RUNX3 in Gastric Epithelial Cells

Claudin-1 Has Tumor Suppressive Activity and Is a Direct Target of RUNX3 in Gastric Epithelial Cells

RUNX3 is multifunctional in carcinogenesis of multiple solid tumors

Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer

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