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野黄芩苷通过下调 JAK2/STAT3 通路抑制肝癌细胞的增殖和侵袭。

Scutellarin inhibits proliferation and invasion of hepatocellular carcinoma cells via down-regulation of JAK2/STAT3 pathway.

机构信息

Department of Breast Surgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

J Cell Mol Med. 2019 Apr;23(4):3040-3044. doi: 10.1111/jcmm.14169. Epub 2019 Jan 29.

DOI:10.1111/jcmm.14169
PMID:30697962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6433857/
Abstract

The prognosis of hepatocellular carcinoma (HCC) is poor because of high incidence of recurrence and metastasis. JAK/STAT signalling pathway regulates cell proliferation, apoptosis, differentiation and migration and epithelial-mesenchymal transition (EMT) is also considered to contribute to invasion and metastasis of epithelial malignant tumours. Scutellarin is an active component found in many traditional Chinese herbs and has been regularly used in anti-inflammatory and antitumour medicine. This study aimed to identify the effect of scutellarin and its possible mechanism of action in HCC cells. Proliferation, colony-forming, apoptosis and cell migration assays were used to examine the effect of scutellarin on HCC cells. Quantitative real-time PCR and Western blotting were performed to study the molecular mechanisms of action of scutellarin. Light and electron microscopy and immunofluorescence analysis were performed to study the effect of scutellarin on cellular mechanics. We show that scutellarin potentially suppresses invasiveness of HepG2 and MHCC97-H cells in vitro by remodelling their cytoskeleton. The molecular mechanism behind it might be the inhibition of the EMT process, which could be attributed to the down-regulation of the JAK2/STAT3 pathway. These findings may provide new clinical ideas for the treatment of liver cancer.

摘要

肝细胞癌(HCC)的预后较差,因为其复发和转移的发生率较高。JAK/STAT 信号通路调节细胞增殖、凋亡、分化和迁移,上皮-间充质转化(EMT)也被认为有助于上皮恶性肿瘤的侵袭和转移。野黄芩苷是许多中药中的一种活性成分,已被常规用于抗炎和抗肿瘤药物。本研究旨在确定野黄芩苷对 HCC 细胞的作用及其可能的作用机制。通过增殖、集落形成、凋亡和细胞迁移实验来检测野黄芩苷对 HCC 细胞的影响。通过定量实时 PCR 和 Western blot 分析来研究野黄芩苷的作用机制。通过光镜和电镜以及免疫荧光分析来研究野黄芩苷对细胞力学的影响。我们表明,野黄芩苷可能通过重塑其细胞骨架来抑制 HepG2 和 MHCC97-H 细胞的体外侵袭能力。其潜在的分子机制可能是 EMT 过程的抑制,这可能归因于 JAK2/STAT3 通路的下调。这些发现可能为肝癌的治疗提供新的临床思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0666/6433857/f38529877dda/JCMM-23-3040-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0666/6433857/3ed191584f8d/JCMM-23-3040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0666/6433857/f38529877dda/JCMM-23-3040-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0666/6433857/3ed191584f8d/JCMM-23-3040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0666/6433857/f38529877dda/JCMM-23-3040-g002.jpg

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