Research Paper Volume 11, Issue 13 pp 4407—4437
HNRNPA1-mediated 3′ UTR length changes of HN1 contributes to cancer- and senescence-associated phenotypes
Figure 7. Graphic abstract for HNRNPA1-mediated 3′ UTR length changes contributes to cancer- and senescence-associated phenotypes. In cancer cells, upregulated HNRNPA1 leads to higher usage of proximal pA site of HN1 and thus increases the level of its transcripts with shorter 3′ UTR, which produces more protein than the longer one, and ultimately promotes cancer-associated phenotypes. In senescent cells, HNRNPA1 is downregulated and causes higher usage of distal pA site of HN1. Such regulation lengthens the 3′ UTR of HN1 and generates less protein, which in turn promotes senescence-associated phenotypes in both normal and cancer cells.