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The Links between Transcription, beta-catenin/JNK Signaling, and Carcinogenesis
Molecular Cancer Research, 08/14/09

The authors 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.

Exclusive Author Commentary
Abdolrahman Shams Nateri, 08/18/09

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 normal cells. Currently, our understanding of activated WNTs suggests that these proteins play key assembly functions for promoting efficient protein–protein interaction and stand at the crossroads of several signalling pathways helping to integrate and coordinate the plethora of continuously changing signals. In fact, a Wnt pathway mutation, such as loss of the adenomatous polyposis coli (APC) gene, is sufficient to give rise to a tumour that grows without limit. This suggests that the mutation, through ectopically activating the Wnt pathway, may also switch on associated pathways; Notch, Eph/ephrin, BMP, Hedgehog and MAPK, as observed in the ApcMin mouse model of intestinal carcinogenesis. We have previously demonstrated the importance of links between canonical (?-Catenin/TCF4) and non-canonical (JNK/c-Jun) Wnt signalling pathways in intestinal tumorigenesis. This relationship is supported by recent studies using alternative approaches from others. More recently, we have also shown the physiological importance of activated JNK signalling in intestinal stem cell regulation. Genetic studies in the mouse suggest that these regulators have distinct roles at in early development but may function in related pathways to maintain the developmental potential of adult stem cells and their commitment to cancer. In this scenario, it is likely that the key normal cell regulators ?-catenin/TCF4:JNK/c-Jun modify gene expression, such that the developmental potential of these cells is reactivated. In this article, we have also introduced potential common target genes of TCF4/c-Jun regulators in the context of normal and altered ?-catenin. We currently lack substantial knowledge of specific profile of gene binding regulated by the AP-1/TCF components; c-Jun and TCF4, accompanies the development of the activated Wnt and/or JNK phenotype in a model of intestinal epithelial regulation and/or whether this profile provides a mechanistic basis for the subpopulation of stem cell like phenotype (cancer stem cells) in cancer.

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