The links between transcription, beta-catenin/JNK signaling, and carcinogenesis.
Interactions between transcription and signaling are fundamentally important for understanding both the structure and function of genetic pathways and their role in diseases such as cancer. The finding that beta-catenin/TCF4 and JNK/c-Jun cooperate has important implications in carcinogenesis. Previously, we found that binding of c-Jun and beta-catenin/TCF4 to the c-jun promoter is dependent upon JNK activity, thus one role for this complex is to contribute to the repression and/or activation of genes that may mediate cell maintenance, proliferation, differentiation, and death, whereas deregulation of these signals may contribute to carcinogenesis. Here we address the functional links reported between activated beta-catenin/JNK signaling pathways, their component genes, and their common targets, and discuss how alterations in the properties of these genes lead to the development of cancer.
Saadeddin
Anas
A
Cancer Genetics Group, Division of Pre-Clinical Oncology, NottinghamDigestive Diseases Centre, School of Clinical Sciences, University of Nottingham, Nottingham, United Kingdom. a.nateri@nottingham.ac.uk
Babaei-Jadidi
Roya
R
Spencer-Dene
Bradley
B
Nateri
Abdolrahman Shams
AS
D000818:Animals; D052138:Genes, Neoplasm; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D009369:Neoplasms / Q000201:enzymology* / Q000235:genetics* / Q000378:metabolism; D014158:Transcription, Genetic; D051153:Wnt Proteins / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism*
D051153:Wnt Proteins; D051176:beta Catenin; D048031:JNK Mitogen-Activated Protein Kinases