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. Author manuscript; available in PMC: 2016 Oct 4.
Published in final edited form as: Oncogene. 2016 Apr 4;35(38):5056–5069. doi: 10.1038/onc.2016.67

Figure 10.

Figure 10

Model of inhibition of U2AF2-dependent CD44 alternative splicing by CD82 in metastatic melanoma. Upper panel, in non-metastatic melanoma, expression of CD82 induces ubiquitination and degradation of U2AF2, which leads to exon V8-10 skipping of CD44 pre-mRNA. Lower panel, loss of CD82 expression results in stabilization and binding of U2AF2 to 3’-splicing site of the intron adjacent to exon V8. This process facilitates exon V8-10 splicing, enhances the binding affinity of CD44 to E-selectin and promotes stress fiber formation and Src/FAK/RhoA activation, leading to increased motility and metastatic potential of melanoma.