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首页> 外文期刊>In vivo. >Anticancer Effects of Baicalein in FRO Thyroid Cancer Cells Through the Up-regulation of ERK/p38 MAPK and Akt Pathway
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Anticancer Effects of Baicalein in FRO Thyroid Cancer Cells Through the Up-regulation of ERK/p38 MAPK and Akt Pathway

机译:黄ical素通过上调ERK / p38 MAPK和Akt信号通路对甲状腺癌细胞的抗癌作用

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Background/Aim: The aim of the study was to evaluate the anticancer effects of baicalein in FRO anaplastic thyroid cancer (ATC) cells. Materials and Methods: FRO cells were treated with baicalein and viability was measured by the MTT assay. Cell apoptosis was observed by staining with Hoechst dye. The expression of apoptotic proteins (Bax, Bcl-2, PARP, cytochrome c, and caspase-3) and the inflammatory protein Cox-2 and the phosphorylation of MAPKs and Akt were determined by western blot. Results: Treatment with baicalein inhibited cell proliferation in a time-dependent manner and increased DNA fragmentation and apoptosis in FRO cells. Baicalein at 50 and 100 M inhibited the expression of Bax, PARP, cytochrome c, cleaved caspase-3, and Cox-2, and increased the expression of Bcl-2. Baicalein increased the phosphorylation of ERK, p38 MAPK, and Akt and decreased JNK phosphorylation. Conclusion: Baicalein caused anticancer effects in FRO ATC cells through induction of apoptosis and regulation of the MAPK and Akt pathway.
机译:背景/目的:本研究的目的是评估黄ical素对FRO变性甲状腺癌(ATC)细胞的抗癌作用。材料与方法:用黄ical苷处理FRO细胞,并通过MTT测定法测定生存力。通过用Hoechst染料染色观察到细胞凋亡。通过蛋白质印迹法检测凋亡蛋白(Bax,Bcl-2,PARP,细胞色素c和胱天蛋白酶3)的表达以及炎性蛋白Cox-2的表达以及MAPKs和Akt的磷酸化。结果:黄ical苷以时间依赖性方式抑制细胞增殖,并增加FRO细胞的DNA片段化和凋亡。黄ical素在50和100 M时抑制Bax,PARP,细胞色素c,裂解的caspase-3和Cox-2的表达,并增加Bcl-2的表达。黄ical素增加ERK,p38 MAPK和Akt的磷酸化,并降低JNK的磷酸化。结论:黄ical苷通过诱导细胞凋亡以及调控MAPK和Akt途径对FRO ATC细胞产生抗癌作用。

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