Apigenin facilitates apoptosis of acute lymphoblastic leukemia cells via AMP-activated protein kinase-mediated ferroptosis  

作　　者：CANCAN HE TINGTING ZHANG WEI XIONG SHENGYU WANG XIN SUN 

机构地区：[1]Department of Pediatrics,Affiliated Hospital of Zunyi Medical University,Zunyi,563003,China [2]Department of Pediatrics,Guizhou Children’s Hospital,Zunyi,563003,China [3]Department of Radiology,Affiliated Hospital of Zunyi Medical University,Zunyi,563003,China [4]Department of Cardiovascular Surgery,Affiliated Hospital of Zunyi Medical University,Zunyi,563003,China [5]Key Laboratory of Infectious Disease&Biosafety,College of Preclinical Medicine,Zunyi Medical University,Zunyi,563003,China [6]Department of Microbiology,College of Preclinical Medicine,Zunyi Medical University,Zunyi,563003,China

出　　处：《Oncology Research》2025年第2期421-429,共9页肿瘤学研究(英文)

基　　金：supported by The National Natural Science Foundation of China(No.31902283);Research Foundation for Master students at the Affiliated Hospital of Zunyi Medical College(No.22-2018).

摘　　要：Background:The outcomes of pediatric patients with acute lymphoblastic leukemia(ALL)remain far less than favorable.While apigenin is an anti-cancer agent,studies on the mechanism by which it regulates ALL cell cycle progression are inadequate.Ferroptosis and AMP-activated protein kinase(AMPK)signaling are important processes for ALL patients.However,it remains unclear whether apigenin works by affecting AMPK and apoptosis.Materials and Methods:SUP-B15 and T-cell Jurkat ALL cells were treated with apigenin,and cell viability and apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)assays,respectively.The thiobarbituric acid-reactive substances(TBARS)assay was used to evaluate lipid peroxidation.Intracellular Fe2+levels were measured using a commercial kit.Corresponding proteins were detected by western blotting.Results:Results showed that apigenin reduced cell viability and the levels of Ki67 and proliferating cell nuclear antigen(PCNA)expression in a concentration-dependent manner in both types of ALL cells.Apigenin also exerted anti-apoptotic effects on SUP-B15 and Jurkat cells.Apigenin activated AMP-activated protein kinase(AMPK)signaling and induced ferroptosis,and those effects were attenuated by inhibition of AMPK.Eventually,the reduced cell proliferation and increased cell apoptosis caused by apigenin in ALL cells were partly abolished by AMPK inhibition.Conclusion:In summary,apigenin exerted anti-leukemia activity in ALL cells,and that effect was partially achieved by activation of AMPK signaling.Our findings suggest apigenin as a potential drug for treatment of ALL.

关 键 词：Acute lymphoblastic leukemia(ALL) APIGENIN APOPTOSIS AMP-activated protein kinase(AMPK) Ferroptosis 

分 类 号：R733.71[医药卫生—肿瘤]