Abstract
To support proliferation, tumour cells often undergo a metabolic switch to aerobic glycolysis, and a large amount of fatty acids (FAs) is produced to provide conditions for the formation of cell membrane structures. This phenomenon is particularly prominent in clear cell renal cell carcinoma (ccRCC). FAs need to be combined with fatty acid binding proteins (FABPs) for transport. Fatty Acid Binding Protein 5 (FABP5) is an important chaperone protein of FAs that is upregulated in a variety of tumours. However, to date, the potential regulatory role and molecular mechanisms of FABP5 in the development and progression of cancers, including ccRCC, remain unknown. Herein, we demonstrate that FABP5 is upregulated in human ccRCC tissues and cell lines and is positively correlated with the progression of ccRCC. FABP5 deletion inhibits the proliferation, colony-forming ability and migration of ccRCC cells, suggesting that FABP5 may be a cancer-promoting protein in ccRCC. Mechanistically, FABP5 deletion significantly downregulated MMP9 and the transcription factor Snail1 in addition to upregulating E-cadherin and downregulating N-cadherin and Vimentin to inhibit epithelial-mesenchymal transition (EMT) in the ACHN cell line. In summary, our data suggest that FABP5 may be a potential therapeutic target in ccRCC.