TY - JOUR
T1 - A knotty turnabout? Akt1 as a metastasis suppressor
AU - Wyszomierski, Shannon L.
AU - Yu, Dihua
PY - 2005/12
Y1 - 2005/12
N2 - Akt is well known to enhance malignancy and is recognized as a key target for antineoplastic therapies. However, intriguing findings reported by Yoeli-Lerner et al. in the November 23, 2005 issue of Molecular Cell, suggest a novel, antimetastasis function of Akt: activation of Akt1 inhibited invasion in some cancer cells. One possible mechanism for this surprising phenotype was that Akt activated the E3 ubiquitin ligase HDM2, causing ubiquitination and degradation of NFAT, an invasion-promoting factor. These findings clearly justify further investigations and, if validated in vivo, call for reevaluation of some Akt-targeting therapeutic strategies currently under development.
AB - Akt is well known to enhance malignancy and is recognized as a key target for antineoplastic therapies. However, intriguing findings reported by Yoeli-Lerner et al. in the November 23, 2005 issue of Molecular Cell, suggest a novel, antimetastasis function of Akt: activation of Akt1 inhibited invasion in some cancer cells. One possible mechanism for this surprising phenotype was that Akt activated the E3 ubiquitin ligase HDM2, causing ubiquitination and degradation of NFAT, an invasion-promoting factor. These findings clearly justify further investigations and, if validated in vivo, call for reevaluation of some Akt-targeting therapeutic strategies currently under development.
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U2 - 10.1016/j.ccr.2005.11.006
DO - 10.1016/j.ccr.2005.11.006
M3 - Short survey
C2 - 16338656
AN - SCOPUS:28844490209
SN - 1535-6108
VL - 8
SP - 437
EP - 439
JO - Cancer cell
JF - Cancer cell
IS - 6
ER -