Figure 6. A working model for SRSF3-mediated 3′ UTR shortening contributes to cellular senescence. SRSF3 prefers proximal pA sites binding and represses nearby pA sites usage in target genes such as PTEN, PIAS1 and DNMT3A in normal conditions. Upon SRSF3 knockdown, the repression effect reduced, which in turn leads to the higher usage of corresponding pA sites and 3′ UTR shortening of target genes. Transcripts with shortened 3′ UTR generate more protein, possibly by escaping the miRNA targeting, and finally lead to senescence-associated phenotypes.