结直肠癌
癌症研究
转移
活力测定
长非编码RNA
生物
小RNA
核糖核酸
体内
分子生物学
竞争性内源性RNA
报告基因
癌症
细胞培养
基因表达
基因
遗传学
作者
Jianfeng Li,Yeyu Qin,Weijun Wang,Kai Yang,Min Zhang
出处
期刊:Anti-Cancer Drugs
[Ovid Technologies (Wolters Kluwer)]
日期:2020-07-28
卷期号:32 (2): 148-156
被引量:10
标识
DOI:10.1097/cad.0000000000000981
摘要
Colorectal cancer (CRC) is a commonly diagnosed type of cancer globally. The molecular mechanism by which peiminine suppressed the progression of CRC is not fully addressed. The viability was assessed through cell counting kit 8 assay. Colony formation assay was used to analyze the colony formation ability. The metastasis was evaluated by transwell migration and invasion assays. Quantitative real-time PCR was performed to measure the expression of LINC00659 and miR-760 in CRC cells. The binding sites between miR-760 and LINC00659 were predicted by Starbase software and verified by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA-pull down assay. The in-vivo function of peiminine in CRC progression was confirmed by murine xenograft model. Peiminine inhibited the viability, colony formation and metastasis of CRC cells. Peiminine notably down-regulated the expression of LINC00659, while the expression of miR-760 was up-regulated by peiminine treatment. MiR-760 was a direct target of LINC00659 in CRC cells. The depletion of miR-760 attenuated the inhibitory effects of LINC00659 intervention on the viability, colony formation and metastasis of CRC cells. Peiminine restrained the progression of CRC through LINC00659 and miR-760. LINC00659 inhibited the growth of CRC tumors through LINC00659/miR-760 axis in vivo. Peiminine suppressed the development of CRC through inhibiting the viability, colony formation and metastasis of CRC cells via LINC00659/miR-760 axis. LINC00659/miR-760 axis might be an underlying target for CRC therapy.
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