| Literature DB >> 31787239 |
Tomohiro Yoshida1, Shingo Yamasaki1, Osamu Kaneko1, Naofumi Taoka1, Yusuke Tomimoto1, Ichiji Namatame1, Toshiko Yahata1, Sadao Kuromitsu1, Lewis C Cantley2, Costas A Lyssiotis3.
Abstract
Metabolic programs are rewired in cancer cells to support survival and tumor growth. Among these, recent studies have demonstrated that glutamate-oxaloacetate transaminase 1 (GOT1) plays key roles in maintaining redox homeostasis and proliferation of pancreatic ductal adenocarcinomas (PDA). This suggests that small molecule inhibitors of GOT1 could have utility for the treatment of PDA. However, the development of GOT1 inhibitors has been challenging, and no compound has yet demonstrated selectivity for GOT1-dependent cell metabolism or selective growth inhibition of PDA cell lines. In contrast, potent inhibitors that covalently bind to the transaminase cofactor pyridoxal-5'-phosphate (PLP), within the active site of the enzyme, have been reported for kynurenine aminotransferase (KAT) and gamma-aminobutyric acid aminotransferase (GABA-AT). Given the drug discovery successes with these transaminases, we aimed to identify PLP-dependent suicide substrate-type GOT1 inhibitors. Here, we demonstrate that PF-04859989, a known KAT2 inhibitor, has PLP-dependent inhibitory activity against GOT1 and shows selective growth inhibition of PDA cell lines.Entities:
Keywords: Aminotransferase; GOT1; Metabolism; PLP; Pancreatic cancer; Transaminase
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Year: 2019 PMID: 31787239 PMCID: PMC6981064 DOI: 10.1016/j.bbrc.2019.11.130
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575