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黄芩苷通过抑制蛋白激酶 C/信号转导和转录激活因子 3(PKC/STAT3)信号通路抑制人宫颈癌细胞。

Baicalin Inhibits Human Cervical Cancer Cells by Suppressing Protein Kinase C/Signal Transducer and Activator of Transcription (PKC/STAT3) Signaling Pathway.

机构信息

Department of Gynecology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, China (mainland).

People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China (mainland).

出版信息

Med Sci Monit. 2018 Apr 3;24:1955-1961. doi: 10.12659/msm.909640.

DOI:10.12659/msm.909640
PMID:29610452
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5896362/
Abstract

BACKGROUND Like other human cancers, the malignancy of cervical cancer is also characterized by abilities of proliferation, migration, and invasion. Protein kinase C-zeta (PKCζ) has been highly correlated with several human cancers. Baicalin was proven to regulate PKC. This study aimed to investigate the anti-cancer effect and involved molecular mechanisms of baicalin on human cervical cancer. MATERIAL AND METHODS Baicalin at various concentrations was used to treat 2 human cervical cancer cell lines HeLa and SiHa. The proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenylterazolium bromide (MTT) assay. The apoptosis was detected by terminal transferase UTP nick end labeling (TUNEL) assay. Wound healing assay and Transwell assay were used to evaluate the migration and invasion respectively. Western blotting was performed to assess the protein expression levels. RESULTS Baicalin administration significantly reduced the viability by facilitating the apoptosis in HeLa and SiHa cells. Baicalin treatment also significantly reduced the wound closure and cell amount invaded as measured by Transwell assay. The expression levels of PKCζ, survivin, matrix metalloproteinase (MMP)2, MMP9 as well as the phosphorylation of signal transducer and activator of transcription (STAT) 3 were reduced in baicalin administrated cervical cancer cells. CONCLUSIONS Baicalin exerted anti-cancer effects on human cervical cancer cells by targeting STAT3 regulated signaling pathways.

摘要

背景

与其他人类癌症一样,宫颈癌的恶性特征还表现在增殖、迁移和侵袭能力上。蛋白激酶 C-ζ(PKCζ)与多种人类癌症高度相关。黄芩素已被证明可调节 PKC。本研究旨在探讨黄芩素对人宫颈癌的抗癌作用及相关分子机制。

材料与方法

用不同浓度的黄芩素处理 2 个人宫颈癌细胞系 HeLa 和 SiHa。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴盐(MTT)法评估增殖。末端转移酶 UTP 缺口末端标记(TUNEL)法检测凋亡。划痕愈合试验和 Transwell 试验分别用于评估迁移和侵袭。通过 Western blot 检测蛋白表达水平。

结果

黄芩素给药通过促进 HeLa 和 SiHa 细胞凋亡,显著降低细胞活力。黄芩素处理还显著减少了 Transwell 试验中测量的伤口闭合和细胞侵袭数量。黄芩素处理的宫颈癌细胞中 PKCζ、survivin、基质金属蛋白酶(MMP)2、MMP9 的表达水平以及信号转导和转录激活因子 3(STAT3)的磷酸化水平降低。

结论

黄芩素通过靶向 STAT3 调节的信号通路对人宫颈癌细胞发挥抗癌作用。

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