Phosphatidylcholine-Specific Phospholipase C as a Promising Drug Target
Issued Date
2023-08-01
Resource Type
eISSN
14203049
Scopus ID
2-s2.0-85167771470
Pubmed ID
37570610
Journal Title
Molecules
Volume
28
Issue
15
Rights Holder(s)
SCOPUS
Bibliographic Citation
Molecules Vol.28 No.15 (2023)
Suggested Citation
Eurtivong C., Leung E., Sharma N., Leung I.K.H., Reynisson J. Phosphatidylcholine-Specific Phospholipase C as a Promising Drug Target. Molecules Vol.28 No.15 (2023). doi:10.3390/molecules28155637 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/88839
Title
Phosphatidylcholine-Specific Phospholipase C as a Promising Drug Target
Author(s)
Other Contributor(s)
Abstract
Phosphatidylcholine-specific phospholipase C (PC-PLC) is an enzyme that catalyzes the formation of the important secondary messengers phosphocholine and diacylglycerol (DAG) from phosphatidylcholine. Although PC-PLC has been linked to the progression of many pathological conditions, including cancer, atherosclerosis, inflammation and neuronal cell death, studies of PC-PLC on the protein level have been somewhat neglected with relatively scarce data. To date, the human gene expressing PC-PLC has not yet been found, and the only protein structure of PC-PLC that has been solved was from Bacillus cereus (PC-PLCBc). Nonetheless, there is evidence for PC-PLC activity as a human functional equivalent of its prokaryotic counterpart. Additionally, inhibitors of PC-PLCBc have been developed as potential therapeutic agents. The most notable classes include 2-aminohydroxamic acids, xanthates, N,N′-hydroxyureas, phospholipid analogues, 1,4-oxazepines, pyrido[3,4-b]indoles, morpholinobenzoic acids and univalent ions. However, many medicinal chemistry studies lack evidence for their cellular and in vivo effects, which hampers the progression of the inhibitors towards the clinic. This review outlines the pathological implications of PC-PLC and highlights current progress and future challenges in the development of PC-PLC inhibitors from the literature.