LPCAT1 depletion inhibits colorectal cancer tumorigenesis and is associated with the ECM-receptor-interaction signaling pathway

Colorectal cancer (CRC) has become one of the most important diseases due to its increasing morbidity and mortality. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is reported to be overexpressed in multiple cancers, but their role remains poorly understood. In this study, we explored the role of LPCAT1 in the progression of CRC and the possible underlying mechanism. Bioinformatics analysis was used to search for the association between target gene LPCAT1 and CRC. LPCAT1 expression was measured in CRC and paired para cancerous tissues. The role of LPCAT1 was investigated both in vitro and in vivo. iTRAQ-based quantitative proteomics was used to explore the mechanism of LPCAT1 in CRC progression. TCGA and GEO database analysis showed that LPCAT1 was upregulated in CRC. LPCAT1 was upregulated in CRC tissues and the IHC score was also correlated with tumor stage. The depletion of LPCAT1 not only abrogated cell proliferation, migration and invasion in vitro, but also arrested tumor growth in vivo. The proteomic results showed that differentially expressed proteins were enriched in multiple pathways after LPCAT1 knockdown, and the extracellular matrix (ECM) receptor interaction pathway was the most significant. The ECM is involved in the process by which LPCAT1 promotes CRC metastasis and invasion.