A549电池
基因敲除
细胞凋亡
己糖激酶
糖酵解
顺铂
细胞生长
转染
下调和上调
细胞生物学
癌症研究
化学
癌细胞
生物
分子生物学
细胞培养
生物化学
癌症
新陈代谢
化疗
基因
遗传学
作者
Shishun Xie,Xiangjun Li,Jianjun Zhao,Zhimin Fan,zhiyun shu,Hongyan Cheng,Siyao Liu,Sien Shi
摘要
Abstract Background Hexokinase (HK) is the first rate‐limiting enzyme of glycolysis, which can convert glucose to glucose‐6‐phosphate. There are several subtypes of HK, including HK2, which is highly expressed in a variety of different tumors and is closely associated with survival. Methods Non‐small cell lung cancer (NSCLC) A549 cells with stable overexpression and knockdown of HK2 were obtained by lentivirus transfection. The effects of overexpression and knockdown of HK2 on proliferation, migration, invasion, and glycolytic activity of A549 cells were investigated. The effects on apoptosis were also analyzed using western blot and flow cytometry. In addition, the mitochondria and cytoplasm were separated and the expression of apoptotic proteins was detected by western blot respectively. Results Upregulation of HK2 could promote glycolysis, cell proliferation, migration, and invasion, which would be inhibited through the knockdown of HK2. HK2 overexpression contributed to cisplatin resistance, whereas HK2 knockdown enhanced cisplatin‐induced apoptosis in A549 cells. Conclusions Overexpression of HK2 can promote the proliferation, migration, invasion, and drug resistance of A549 cells by enhancing aerobic glycolysis and inhibiting apoptosis. Reducing HK2 expression or inhibiting HK2 activity can inhibit glycolysis and induce apoptosis in A549 cells, which is expected to be a potential treatment method for NSCLC.
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