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. 2018 May 1;9(33):22929–22944. doi: 10.18632/oncotarget.25149

Figure 7. Cyclin E expression in ESCC in terms of the potential interaction between FIR/FIRΔexon2 and FBW7.

Figure 7

The extent of mRNA suppression of Notch1 and cyclin E by SAP155 siRNA was different depending on the TP53 expression in ESCC cells. Since SAP155 is required for proper alternative splicing of FIR (PUF60) pre-mRNA, knockdown of SAP155 recovered FBW7 function possibly by reducing FIR/FIRΔexon2 expression. Therefore, the function rather than the expression of FBW7 was obstructed directly or indirectly by reduced SAP155 expression. The AS form of FIR, FIRΔexon2, inhibits FBW7 function in esophageal cancer cells. Note, the knockdown of SAP155 (SF3b1) expression induced the decrease of Notch1 and cyclin E, which are substrates of FBW7. SAP155 siRNA rescued FBW7 function by potentially reducing FIR/FIRΔexon2 expression. Three-dimensional structure analysis revealed that a WD-like motif exists on the degron pocket of FBW7 protein that potentially interacts with FIR/FIRΔexon2 (see text).