PARP1 is involved in base excision repair (BER), single- and double-strand break repair, and chromosomal stability. It is also involved in transcriptional regulation through its facilitation of protein–protein interactions. PARP1 uses NAD in order to perform its function in apoptosis. If a PARP becomes overactive the cell will have decreased levels of NAD cofactor as well as decreased levels of ATP and thus will undergo necrosis. This is important in carcinogenesis because it could lead to the selection of PARP1 deficient cells (but not depleted) due to their survival advantage during cancer growth.
Susceptibility to carcinogenesis under PARP1 deficiency depends significantly on the type of DNA damage incurred. There are many implications that various PARPs are involved in preventing carcinogenesis. As stated previously, PARP1 and PARP2 are involved in BER and chromosomal stability. PARP3 is involved in centrosome regulation. Tankyrase is another (ADP-ribosyl)polymerase that is involved in telomere length regulation.
PARP1 inhibition has also been widely studied in anticancer therapeutics. The mechanism of action of a PARP1 inhibitor is to enhance the damage done by chemotherapy on the cancerous DNA by disallowing the reparative function of PARP1 in BRCA1/2 deficient individuals .
PARP14 is another ADP-ribosylating enzyme that has been well-studied in regards to cancer therapy targets; it is a signal transducer and activator of STAT6 transcription-interacting protein, and was shown to be associated with the aggressiveness of B-cell lymphomas.