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MST1-JNK信号通路在牛磺酸诱导的结肠癌细胞凋亡中的作用

Roles of the MST1-JNK signaling pathway in apoptosis of colorectal cancer cells induced by Taurine.

作者信息

Liu Zhuoqi, Xia Yanqin, Zhang Xiali, Liu Liqiao, Tu Shuo, Zhu Weifeng, Yu Lehan, Wan Huifang, Yu Bo, Wan Fusheng

机构信息

a Department of Biochemistry and Molecular Biology , School of Basic Medical Sciences, Nanchang University , Nanchang China.

b Laboratory Animal Science Center , Nanchang University , Nanchang , China.

出版信息

Libyan J Med. 2018 Dec;13(1):1500346. doi: 10.1080/19932820.2018.1500346.

Abstract

The aim of this study was to observe the impact of the mammalian sterile 20-like kinase 1-c-Jun N-terminal kinase (MST1-JNK) signaling pathway on apoptosis in colorectal cancer (CRC) cells induced by Taurine (Tau). Caco-2 and SW620 cells transfected with p-enhanced green fluorescent protein (EGFP)-MST1 or short interfering RNA (siRNA)-MST1 were treated with Tau for 48 h. Apoptosis was detected by flow cytometry, and the levels of MST1 and JNK were detected by western blotting. Compared with the control group, 80 mM Tau could significantly induce apoptosis of CRC cells, and the apoptotic rate increased with increasing Tau concentration (P < 0.01). Meanwhile, the protein levels of MST1 and phosphorylated (p)-JNK in Caco-2 cells increased significantly (P < 0.01). The apoptotic rate of the p-EGFP-MST1 plasmid-transfected cancer cells was significantly higher than that of the control group (P < 0.05); however, the apoptotic rate of the p-EGFP-MST1+Tau group was increased further (P < 0.01). Silencing the MST1 gene could decrease the apoptotic rate of cancer cells, and Tau treatment could reverse this decrease. Blocking the JNK signaling pathway significantly reduced the Tau-induced apoptotic rate of CRC cells. Thus, the MST1-JNK pathway plays an important role in Tau-induced apoptosis of CRC cells.

摘要

本研究旨在观察哺乳动物不育20样激酶1 - c - Jun氨基末端激酶(MST1 - JNK)信号通路对牛磺酸(Tau)诱导的结直肠癌(CRC)细胞凋亡的影响。用p - 增强型绿色荧光蛋白(EGFP) - MST1或小干扰RNA(siRNA) - MST1转染的Caco - 2和SW620细胞用Tau处理48小时。通过流式细胞术检测细胞凋亡,通过蛋白质印迹法检测MST1和JNK的水平。与对照组相比,80 mM Tau可显著诱导CRC细胞凋亡,且凋亡率随Tau浓度增加而升高(P < 0.01)。同时,Caco - 2细胞中MST1和磷酸化(p) - JNK的蛋白水平显著升高(P < 0.01)。p - EGFP - MST1质粒转染的癌细胞凋亡率显著高于对照组(P < 0.05);然而,p - EGFP - MST1 + Tau组的凋亡率进一步升高(P < 0.01)。沉默MST1基因可降低癌细胞凋亡率,而Tau处理可逆转这种降低。阻断JNK信号通路显著降低了Tau诱导的CRC细胞凋亡率。因此,MST1 - JNK通路在Tau诱导的CRC细胞凋亡中起重要作用。

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