Gambogic acid induces death of K562 cells through autophagy and apoptosis mechanisms

被引：9

作者：

Chen, Jinhao ^{[1
]}

Zhou, Min ^{[1
]}

Zhang, Qian ^{[1
]}

Xu, Jingyan ^{[1
]}

Ouyang, Jian ^{[1
]}

机构：

[1] Nanjing Univ, Sch Med, Nanjing Drum Tower Hosp, Dept Hematol,Affiliated Hosp, Nanjing 210008, Jiangsu, Peoples R China

来源：

LEUKEMIA & LYMPHOMA | 2015年 / 56卷 / 10期

关键词：

Gambogic acid; chronic myelogenous leukemia; autophagy; apoptosis; CHRONIC MYELOID-LEUKEMIA; BCR-ABL; BLAST CRISIS; IMATINIB; BCL-2; INHIBITION; INSIGHTS; GROWTH; PHASE; BAX;

D O I：

10.3109/10428194.2015.1018251

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

This study was aimed to detect the effects of gambogic acid (GA) on the growth of chronic myelogenous leukemia (CML) K562 cells. Our results showed that GA induced the accumulation of autophagic vacuoles and up-regulation of two autophagy-related proteins (Beclin 1 and LC3). GA also induced down-regulation of mRNA levels of BCR-ABL fusion gene and SQSTM1/sequestosome 1 (p62) protein levels. After treatment by chloroquine (CQ) and pan caspase inhibitor Z-VAD-FMK (PC), both GA-induced autophagy and apoptosis were inhibited. Our study demonstrates that GA may induce cell death through autophagy and apoptosis pathways in CML K562 cells. A cross-talk mechanism exists between GA-induced autophagy and apoptosis. However, the mechanism of GA for inducing autophagy and apoptosis need further clarification.

引用

页码：2953 / 2958

页数：6

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