Signalling Pathways of β-Catenin/JNK in Carcinogenesis

摘要: Tight control of signalling/transcriptional activity ensures that the correct balance between gene expression changes regulating cell cycle, DNA repair, developmental potential and fate determination is maintained by different cells. Activation Wnt signalling pathway stimulates growth mediates carcinogenic In fact, a mutation, such as loss adenomatous polyposis coli gene, sufficient to give rise tumor grows without limit. This suggests through ectopically activating pathway, may also switch on associated pathways; Notch, Eph/ephrin, bone morphogenetic protein, Hedgehog mitogen-activated protein kinase, observed in Apc Min/+ mouse model intestinal carcinogenesis. can activate non-canonical, β-catenin-independent pathways, including activation c-Jun N-terminal kinase (JNK). JNK activation, which occur via many types cellular stress or extracellular signals, plays an essential role organogenesis during development proliferation, survival apoptosis. involved messenger RNA stabilization, migration, cytoskeleton integrity However, links β-catenin pathways are poorly understood, identities downstream targets/effectors Wnt/JNK remain largely unknown. Moreover, little known about effect phosphorylation functions possible common targets these two pathways. chapter discusses relations their identifies component genes