Fig. 5

High ACSL3 expression promotes POPC synthesis to activate PPARα and enhance the transcription of downstream lipid metabolism-associated genes. (A, B) qRT-PCR (A) and western blot (B) analysis of PPARα expression in MHCC-97H and Huh7 cells treated with siACSL3 at a concentration of 30 nM. (C, D) Intracellular concentration of DAG (C) and POPC (D) determined by MS analysis of MHCC-97H and Huh7 cells treated with siACSL3 at a concentration of 30 nM. (E, F) qRT-PCR analysis of the expression of lipid metabolism-associated genes in MHCC-97H (E) and Huh7 cells (F) treated with 30 nM siACSL3 followed by 50 µM POPC. (G, H) ATP production (G) and formation of lipid droplets (H) in MHCC-97H and Huh7 cells treated with 30 nM siACSL3 followed by 50 µM POPC. (I) Schematic illustration of the regulatory mechanism of ACSL3 in promoting HCC growth and metastasis. High ACSL3 expression could promote POPC synthesis to activate PPARα and enhance the transcription of various downstream lipid metabolism-associated genes, which thereby accelerate lipid catabolism and anabolism to promote HCC growth and metastasis. ns, no significance; * p < 0.05; ** p < 0.01; *** p < 0.001