Figure 7. Model for the mechanism by which premature polyadenylation of MAGI3 contributes to malignant transformation.
In normal cells, the proper post-transcriptional processing of transcripts produced by the MAGI3 gene locus gives rise to full-length MAGI3 proteins that negatively regulate the YAP oncoprotein by forming an inhibitory complex. In cancer cells, premature polyadenylation of MAGI3 results in the production of truncated MAGI3 proteins in addition to full-length MAGI3. Truncated MAGI3 is unable to bind YAP but can interact with full-length MAGI3. This dominant-negative interaction may prevent full-length MAGI3 from forming an inhibitory complex with YAP, thus resulting in YAP-mediated malignant transformation.