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黄芩素通过 GSK3β 依赖性途径抑制宫颈癌细胞的增殖。

Baicalein Inhibits the Proliferation of Cervical Cancer Cells Through the GSK3β-Dependent Pathway.

机构信息

Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, P.R. China.

Department of Traditional Chinese Medicine, Yan'an People's Hospital, Yan'an, P.R. China.

出版信息

Oncol Res. 2018 May 7;26(4):645-653. doi: 10.3727/096504017X15031557924141. Epub 2017 Aug 23.

DOI:10.3727/096504017X15031557924141
PMID:28835320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7844692/
Abstract

Baicalein, a flavonoid derived from the root of , has been reported to possess multiple pharmacological activities, such as anticancer and anti-inflammatory properties. This study investigated the effect of baicalein in cervical cancer cells. Cell growth curve and MTT assay were performed and revealed that baicalein inhibited the proliferation of SiHa and HeLa cells in a dose-dependent manner. We further found that baicalein arrested the cell cycle of SiHa and HeLa cells at the G/G phase by suppressing the expression of cyclin D1 through the downregulation of phosphorylated protein kinase B (p-AKT) and phosphorylated glycogen synthase kinase 3β (p-GSK3β) according to FACS assays and Western blotting. Moreover, when CHIR-99021, a GSK3β inhibitor, was added to baicalein-treated SiHa cells, the expression of cyclin D1 was recovered, and cell proliferation was promoted. In conclusion, these data indicated that baicalein suspended the cell cycle at the G/G phase via the downregulation of cyclin D1 through the AKT-GSK3β signaling pathway and further inhibited the proliferation of SiHa and HeLa cervical cancer cells.

摘要

黄芩素是从黄芩根中提取的一种黄酮类化合物，据报道具有多种药理活性，如抗癌和抗炎特性。本研究探讨了黄芩素对宫颈癌细胞的影响。进行了细胞生长曲线和 MTT 测定，结果表明黄芩素呈剂量依赖性抑制 SiHa 和 HeLa 细胞的增殖。我们进一步通过流式细胞术和 Western blot 发现，黄芩素通过下调磷酸化蛋白激酶 B(p-AKT)和磷酸化糖原合成酶激酶 3β(p-GSK3β)抑制 cyclin D1 的表达，将 SiHa 和 HeLa 细胞的细胞周期阻滞在 G1 期。此外，当添加 GSK3β 抑制剂 CHIR-99021 到黄芩素处理的 SiHa 细胞中时，cyclin D1 的表达得到恢复，细胞增殖得到促进。总之，这些数据表明，黄芩素通过 AKT-GSK3β 信号通路下调 cyclin D1 使细胞周期停滞在 G1 期，从而进一步抑制 SiHa 和 HeLa 宫颈癌细胞的增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/6d976819fd9c/OR-26-645-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/84bd91f6a46f/OR-26-645-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/d3712f6c3845/OR-26-645-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/5e566fe00b00/OR-26-645-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/6d976819fd9c/OR-26-645-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/84bd91f6a46f/OR-26-645-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/5ddece232082/OR-26-645-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/d3712f6c3845/OR-26-645-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/5e566fe00b00/OR-26-645-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c32/7844692/6d976819fd9c/OR-26-645-g006.jpg

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