FGF21 levels were independently associated with AMI and may be related to the severity of coronary artery stenosis. Overexpression of FGF21 reduced serum inflammatory factor levels and improved cardiac function in AMI rats.
Mechanistically, exogenous FGF21 treatment enhanced the anti-apoptotic ability of breast cancer cells through STAT3 and Akt/FoXO1 signaling pathways, and mitigated doxorubicin-induced cell death. Furthermore, we observed overexpression of FGF21 in tumor tissues from breast cancer patients, which was associated with poor prognosis. These findings suggest a novel role for FGF21 as an upregulated mediator in the context of NAFLD, promoting breast cancer development and highlighting its potential as a therapeutic target for cancer treatment.
Furthermore, the results revealed that HDAC3 inhibitor‑mediated acetylated modification led to KLB inactivation, resulting in the blockade of FGF21‑KLB signaling, which further triggered the expression of EMT induction‑related genes in Huh7 cells. In conclusion, the present study demonstrated that aberrant acetylated modification of KLB inhibited FGF21‑KLB signaling, thereby promoting β‑catenin signaling‑driven EMT and HCC metastasis.