Cincumol prevents malignant phenotype of colorectal cancer cell line HCT116 via inhibiting PI3K/AKT signaling in vitro.

IF 1.1 4区 医学 Q3 SURGERY
Gaowu Hu, Wenquan Chen, Wei Peng, Zhen Huang, Zhanlin Dong, Yongqing Cao
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Abstract

Purpose: Colorectal cancer (CRC) is a common human cancer along with higher incidence and mortality, and this study aimed to identify the effect of cincumol on CRC and its potential mechanisms.

Methods: CRC cell line HCT116 was used as the material. Cell proliferation was evaluated by CCK-8 assay, and cell migration was detected by scratch test and Transwell assay. TUNEL staining assay was used to evaluate cell apoptosis. The expression of target genes was detected by qualitative real-time polymerase chain reaction and western blot assays.

Results: Cincumol significantly reduced the proliferative and migratory rate and enhanced apoptotic rate of HCT116 cells. Meanwhile, the elevated levels of RBUsuh, Nicd and Tace was also observed in cincumol-treated HCT116 cells. Moreover, our findings revealed that additional cincumol inhibited the expression of p-PI3K and p-AKT, suggesting the inhibition of PI3K/AKT signaling might be involved in the protective role of cincumol on the malignant phenotypes of CRC cells in vitro.

Conclusions: Cincumol inhibited the malignant phenotypes of CRC cells in vitro through inactivating PI3K/AKT signaling, suggesting that cincumol might be a potential anti-CRC agent.

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朱竹酚通过抑制PI3K/AKT信号传导抑制结直肠癌HCT116细胞的恶性表型。
目的:结直肠癌(Colorectal cancer, CRC)是一种发病率和死亡率较高的人类常见癌症,本研究旨在探讨肉桂酚对结直肠癌的影响及其可能的机制。方法:以结直肠癌细胞系HCT116为材料。CCK-8法检测细胞增殖,划痕法和Transwell法检测细胞迁移。TUNEL染色法检测细胞凋亡情况。定量实时聚合酶链反应和western blot检测靶基因的表达。结果:朱竹酚能显著降低HCT116细胞的增殖和迁移率,提高细胞凋亡率。同时,在辛库莫处理的HCT116细胞中,RBUsuh、Nicd和Tace的水平也有所升高。此外,我们的研究结果显示,额外的肉桂酚可以抑制p-PI3K和p-AKT的表达,这表明在体外,肉桂酚对CRC细胞恶性表型的保护作用可能与抑制PI3K/AKT信号通路有关。结论:Cincumol通过灭活PI3K/AKT信号通路,在体外抑制CRC细胞的恶性表型,提示Cincumol可能是一种潜在的抗CRC药物。
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来源期刊
CiteScore
1.90
自引率
9.10%
发文量
60
审稿时长
3-8 weeks
期刊介绍: Information not localized
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