The expression level of lysophosphatidylcholine acyltransferase 1 (LPCAT1) correlates to the progression of prostate cancer

Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

“…However, other studies performed by 31 P-NMR in breast cancer models have reported an increase in these metabolites attributed to increased levels of phospholipase A2 group 4A (47). Lysophosphatidylcholine acyltransferase 1 (LPCAT1) has been studied in colorectal, gastric, and prostate cancers (48)(49)(50) where low plasma levels of these metabolites are associated with the presence of cancer, supporting our preclinical findings. Lysophosphatidylcholines enhance glucose-dependent insulin secretion from pancreatic b-cells and inhibit insulin-induced AKT activation through protein kinase C a in vascular smooth muscle cells (51,52).…”

Mechanism of dihydroartemisinin-induced apoptosis in prostate cancer PC3 cells: An iTRAQ-based proteomic analysis

“…Several proteins are documented to be dyregulated in PCa. LAPCAT1 is overexpressed in PCa, which is associated with advanced cancer stage, high Gleason score, positive nodal involvement, positive surgical margin, and early prostate specific antigen recurrence [58,59]. Elevated serum CKB has been reported in metastatic PCa; moreover, it is associated with poor differentiation of PCa [60][61][62].…”

Lysophospholipid acyltransferases

“…AGPAT2 was also identified as one of the genes which contribute to etoposideinduced cytotoxicity [59]. AGPAT9/LPCAT1 has also recently been shown to be overexpressed in prostate cancer [60]. This increased expression was seen in colorectal adenocarcinomas as well [61].…”