Fig. 7.

NPRA promoted CPT1B expression and tumorigenesis in mice. (A) NPRA knockdown decreased PPARα and CPT1B expression. (B) PPARα knockdown decreased CPT1B expression. (C) By applying si-PPARα to NPRA-overexpressing cells, we found that PPARα and CPT1B expression obviously decreased. (D, E, F) NPRA knockdown MKN45 cells showed decreased tumor formation ability compared with control cells, as reflected by tumor size (D&E) and weight (F). (G) Schematic diagram of the role of NPRA in GC. In conclusion, NPRA activates CPT1B by binding PPARα, which promotes the interaction between NPRA and PPARα proteins in GC, stabilizes the PPARα protein, and promotes the downstream pathway and FAO.