RETRACTED: Alpinumisoflavone exhibits anticancer activities in glioblastoma multiforme by suppressing glycolysis (Retracted Article)

被引:6
作者
Zhao, Xingzhi [1 ]
Zhang, Ting [2 ]
Jiang, Kewei [2 ]
Gao, Heng [1 ]
机构
[1] Nantong Univ, Dept Neurosurg, Jiangyin Peoples Hosp, Wuxi, Jiangsu, Peoples R China
[2] Nantong Univ, Dept Cent Lab, Jiangyin Peoples Hosp, Wuxi, Jiangsu, Peoples R China
来源
ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY | 2020年 / 303卷 / 08期
关键词
Glioblastoma multiforme (GBM); Alpinumisoflavone; glycolysis; HK2; SQUAMOUS-CELL CARCINOMA; FLAVONOIDS; APOPTOSIS; METASTASIS; GROWTH; AXIS;
D O I
10.1002/ar.24242
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Glioblastoma multiforme (GBM, WHO grade IV astrocytoma) has become a public health burden worldwide. Alpinumisoflavone (AIF) is a flavonoid compound isolated from Derris eriocarpa. This study aims to examine the role of AIF in GBM. Our results showed that AIF could decrease the cell viability of both T98G and U373 GBM cell lines. AIF treatment also caused cell cycle arrest at G1/G0 phase along with upregulation of p27 and downregulation of cyclin D1. AIF could significantly induce apoptosis in GBM cells. Activation of caspase-9, disruption of mitochondrial membrane potential and loss of mitochondrial cytochrome C were also observed following AIF treatment. Inhibition of glycolysis by AIF was demonstrated by reducing glucose consumption and lactate output in GBM cells. Moreover, HK2 was identified as the molecular target responsible for the anticancer activities of AIF against GBM cells. The results showed that HK2 knockdown enhanced the anticancer activities of AIF whereas ectopic HK2 expression compromised its effect. Furthermore, the antineoplastic activities of AIF in vivo were also validated in xenograft murine model. Our results showed that AIF can exhibit anticancer activities in GBM by promoting apoptosis and inhibiting glycolysis via targeting HK2. Anat Rec, 2019. (c) 2019 American Association for Anatomy
引用
收藏
页码:2192 / 2201
页数:10
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