CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [PAC-seq]

The goal of this study was to compare globlal poly(A) site usage changes upon CPSF1 knockdown in LNCaP, LNCaP95, and 22Rv1 prostate cancer cells. Overall design: Comparative poly(A) cluster (PAC) profiling in LNCaP, LNCaP95, and 22Rv1 cells between three groups total. LNCaP, LNCaP95, 22Rv1 cells with CPSF1 knocked down via shRNA (shCPSF1-1, shCPSF1-2 and control shCtrl)