CD44细胞
蛋白激酶B
PI3K/AKT/mTOR通路
神经母细胞瘤
小RNA
SH-SY5Y型
下调和上调
癌症研究
细胞生长
细胞凋亡
生物
活力测定
激酶
细胞培养
细胞生物学
信号转导
化学
细胞
基因
生物化学
遗传学
作者
Jing Yang,Xiaojun Shao,Jian Jiang,Yan Sun,Lingzhen Wang,Lirong Sun
摘要
Abstract Neuroblastoma is the most common tumor diagnosed in children and infants, with high recurrence and poor prognosis. Angelica sinensis polysaccharide (AP) whose average molecular weight is 72,900 Da possesses various bioactivities. We aimed to explore the effects of AP on neuroblastoma SH‐SY5Y cells as well as the underlying mechanisms. Effects of AP on cell viability, proliferation, apoptosis, migration, invasion, and expressions of long noncoding RNA H19 (lncRNA‐H19), microRNA (miR)‐675, and CD44 were assessed. Then, effects of miR‐675 overexpression on AP‐treated cells were analyzed. Next, expression of key kinases in the PI3K/AKT and JAK/ STAT pathways was detected. The possible target gene of miR‐675 was finally explored. Cell viability was reduced by 200–500 µg/mL AP. Meanwhile, AP repressed cell proliferation, migration, and invasion, but induced apoptosis. Expressions of lncRNA‐H19 and miR‐675 were upregulated in neuroblastoma cells, and were downregulated by AP. AP was also identified to upregulate CD44. We next found AP affected SH‐SY5Y cells through downregulating miR‐675. Key kinases in the PI3K/AKT and JAK/STAT pathways were downregulated by AP stimulation, while these downregulations were abrogated by miR‐675 overexpression. KIF1B isoform β (KIF1Bβ) is proved to be a target of miR‐675. In conclusion, AP was first identified to inhibit proliferation, migration, and invasion but induce apoptosis. Furthermore, AP might repress tumorigenesis of SH‐SY5Y cells through miR‐675‐mediated inactivation of the PI3K/AKT and JAK/STAT pathways. Besides, KIF1Bβ might be a target of miR‐675.
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