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|Title:||RUNX3 Attenuates β-Catenin/T Cell Factors in Intestinal Tumorigenesis|
|Authors:||Ito, K. |
|Source:||Ito, K., Lim, A.C.-B., Motoda, L., Osato, M., Chuang, L.S.H., Lee, C.W.L., Voon, D.C.-C., Ito, Y., Salto-Tellez, M., Koo, J.K.W., Wang, H., Fukamachi, H. (2008). RUNX3 Attenuates β-Catenin/T Cell Factors in Intestinal Tumorigenesis. Cancer Cell 14 (3) : 226-237. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ccr.2008.08.004|
|Abstract:||In intestinal epithelial cells, inactivation of APC, a key regulator of the Wnt pathway, activates β-catenin to initiate tumorigenesis. However, other alterations may be involved in intestinal tumorigenesis. Here we found that RUNX3, a gastric tumor suppressor, forms a ternary complex with β-catenin/TCF4 and attenuates Wnt signaling activity. A significant fraction of human sporadic colorectal adenomas and Runx3+/- mouse intestinal adenomas showed inactivation of RUNX3 without apparent β-catenin accumulation, indicating that RUNX3 inactivation independently induces intestinal adenomas. In human colon cancers, RUNX3 is frequently inactivated with concomitant β-catenin accumulation, suggesting that adenomas induced by inactivation of RUNX3 may progress to malignancy. Taken together, these data demonstrate that RUNX3 functions as a tumor suppressor by attenuating Wnt signaling. © 2008 Elsevier Inc. All rights reserved.|
|Source Title:||Cancer Cell|
|Appears in Collections:||Staff Publications|
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