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Protein Kinase C in Wnt Signaling: Implications in Cancer Initiation and Progression
被引:27
|作者:
Bernardo Luna-Ulloa, Luis
[1
]
Hernandez-Maqueda, Jose G.
[1
]
Cristina Castaneda-Patlan, M.
[1
]
Robles-Flores, Martha
[1
]
机构:
[1] Univ Nacl Autonoma Mexico, Fac Med, Dept Biochem, Mexico City 04510, DF, Mexico
来源:
关键词:
Wnt signaling;
protein kinase C;
cancer;
cancer progression;
carcinogenesis;
GLYCOGEN-SYNTHASE KINASE-3-BETA;
WNT/BETA-CATENIN;
BETA-CATENIN;
PKC-DELTA;
PATHWAY;
ZETA;
PHOSPHORYLATION;
INHIBITION;
XENOPUS;
PROLIFERATION;
D O I:
10.1002/iub.559
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Although it is well known that Wnt and protein kinase C (PKC) signaling pathways are both involved in carcinogenesis and tumor progression, their synergistic contribution to these processes or the crosstalk between them has just recently been approached. The Wnt and PKC signaling are involved in many cellular functions including proliferation, differentiation, survival, apoptosis, cytoskeletal remodeling, and cell motility. Canonical Wnt signaling has been well characterized as one of the most important contributors to tumorigenesis, and it has been implicated in many types of solid tumors. PKC is one of the key targets of noncanonical Wnt signaling, particularly in the Wnt/Ca2+ pathway. Recently, data have implicated components of noncanonical Wnt/Ca2+ and Wnt/planar cell polarity signaling in directly promoting the invasiveness and malignant progression of diverse forms of human cancer. But, unlike the canonical pathway, defining the roles of noncanonical Wnt signaling in human cancer is in its infancy. In this review, we provide a concise description of the current knowledge of the interaction between PKC and Wnt pathways and discuss the role of this crosstalk in cancer initiation and progression. (C) 2011 IUBMB IUBMB Life, 63(10): 915-921, 2011
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页码:915 / 921
页数:7
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