Proliferating Cell Nuclear Antigen (PCNA) is a DNA polymerase processivity factor essential in both DNA-replication and -repair.1 PCNA is upregulated in a number of conditions where there is mis-regulation of DNA-replication and -repair, such as cancer, thus presenting an attractive inhibition target.2 A 22mer peptide derived from the native PCNA inhibitor, p21, binds to PCNA with the highest affinity known and disrupts PCNA dependent DNA replication.3 This 22mer is cell permeable, however lacks nuclear localisation capability. Here, the 22mer peptide sequence has been optimised to the shortest length while maintaining cell permeability. Fluorescently tagged-peptide sequences 143RQTSMTDFYHSKRR156, 140RKRRQTSMTDFYHSK154 and 140RKRRQTSMTDFYHSKRR156 were synthesised by Solid Phase Peptide Synthesis and cell permeability assayed in breast and prostate cancer cell lines. Increasing the cationic charge by addition of the native arginine residues was necessary for cell permeability.
p21 peptide derivatives are particularly susceptible to aspartimide formation despite the bulky phenylalanine residue neighbouring the aspartic acid. Short, consecutive deprotections with the addition of acids HOBt or formic acid was found necessary to minimise aspartimide formation. Here, the optimised conditions for synthesis of p21 is presented.
NLS (Nuclear Localisation Sequence) tags derived from SV40, cMyc and TAT proteins as well as the synthetic mimetic of penetratin, R6W3, were then conjugated to the cell permeable p21 sequence. These conjugate peptides were effective at translocating to the nucleus and inhibiting PCNA ex vivo. Colocalisation of the NLS tagged peptides and nucleus was observed by confocal microscopy.
This study presents a promising advance in therapeutic peptide development for disruption of PCNA-protein interactions to shut down DNA-replication. Optimisation of the p21 sequence for cell permeability and nuclear localisation allows for direct inhibition of PCNA, carrying many potential applications including development of broad spectrum cancer therapeutics.