A novel polymerase β inhibitor from phage displayed peptide library augments the anti-tumour effects of temozolomide on colorectal cancer.

The therapeutic efficacy of TMZ, a common used drug for chemotherapy, is limited by the resistance from colorectal cancer cells. Base excision repair (BER) pathway has been identified as one of the reasons for drug resistance. By blocking Polβ-dependent BER (Base Excision Repair) pathway, the efficacy of TMZ treatment can be improved greatly.

FEN1 inhibitor synergizes with low-dose camptothecin to induce increased cell killing via the mitochondria mediated apoptotic pathway.

Camptothecin has been used in tumor therapy for a long time but its antitumor effect is rather limited due to the side effect and the drug resistance. FEN1, a major component of DNA repair systems, plays important roles in maintaining genomic stability via DNA replication and repair. Here we found that FEN1 inhibitor greatly sensitizes cancer cells to low-dose camptothecin.

PRMT1 is critical to FEN1 expression and drug resistance in lung cancer cells.

The up-regulation of PRMT1 is critical to the cell growth and cancer progression of lung cancer cells. In our research, we found that PRMT1 is important to the DNA repair ability and drug resistance of lung cancer cells. To demonstrate the functions of PRMT1, we identified Flap endonuclease 1 (FEN1) as a post-translationally modified downstream target protein of PRMT1.