FATP2 regulates non-small cell lung cancer by mediating lipid metabolism through ACSL1

Lipid metabolism is believed to play an important role in cancer. This study aimed to investigate the role and possible mechanism of fatty acid transporter protein 2 (FATP2) in non-small cell lung cancer (NSCLC). FATP2 expression and its relationship with NSCLC prognosis were analyzed using the TCGA database. The si-RNA was used to intervene FATP2 in NSCLC cells, and the effects of si-FATP2 on cell proliferation, apoptosis, lipid deposition, endoplasmic reticulum (ER) morphology, and the proteins expressions of fatty acid metabolism and ER stress were analyzed. In addition, Co-IP analyzed the interaction between FATP2 and ACSL1, and further analyzed the possible mechanism of FATP2 in regulating lipid metabolism using pcDNA-ACSL1. Results found that FATP2 was overexpressed in NSCLC and associated with poor prognosis. Si-FATP2 significantly inhibited the proliferation and lipid metabolism of A549 and HCC827 cells, and induced ER stress to promote apoptosis. Further studies confirmed the protein interaction between FATP2 and ACSL1. Si-FATP2 and pcDNA-ACSL1 co-transfection further inhibit the proliferation and lipid deposition of NSCLS cells, and promote the decomposition of fatty acids. In conclusion, FATP2 promoted the progression of NSCLC by regulating lipid metabolism through ACSL1.

Automated summary

This study investigated the role and mechanism of FATP2 in non-small cell lung cancer (NSCLC) and found that FATP2 was overexpressed in NSCLC and associated with poor prognosis. Inhibition of FATP2 suppressed cell proliferation and lipid metabolism in NSCLC cells, and induced ER stress to promote apoptosis. The study also revealed a protein interaction between FATP2 and ACSL1, suggesting that FATP2 regulates lipid metabolism in NSCLC through ACSL1.