This is a follow-up of sorts to a previous essay on the subject of alternative polyadenylation. In the previous report, I discussed some bioinformatics studies that suggested that the 3′ UTRs of mRNAs change, in bulk, in the course of development in mammals. The implication of these results is that poly(A) site choice in mammals is regulated, with important functional consequences.
A more recent study by Mayr and Bartel adds to this notion. These authors studied 3′ UTR length in normal and cancer cells, and found a striking correlation between 3′ UTR length and the expression of oncogenes. Specifically, higher expression (as is found in cancer cells) is correlated with shorter 3′ UTR. As 3′ UTR length is determined by the position of the poly(A) site along a transcript, this implicates alternative polyadenylation as one mechanism by which oncogene expression is activated.