Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ccr.2008.08.004
Title: RUNX3 Attenuates β-Catenin/T Cell Factors in Intestinal Tumorigenesis
Authors: 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.
Keywords: CELLCYCLE
SIGNALING
Issue Date: 2008
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
URI: http://scholarbank.nus.edu.sg/handle/10635/33193
ISSN: 15356108
DOI: 10.1016/j.ccr.2008.08.004
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