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天然类黄酮非瑟酮通过调节多种信号通路抑制肝癌、结直肠癌和胰腺癌细胞的细胞增殖。

The Natural Flavonoid Fisetin Inhibits Cellular Proliferation of Hepatic, Colorectal, and Pancreatic Cancer Cells through Modulation of Multiple Signaling Pathways.

作者信息

Youns Mаhmoud, Abdel Halim Hegazy Wael

机构信息

Department of Functional Genome Analysis, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, Heidelberg, Germany.

Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.

出版信息

PLoS One. 2017 Jan 4;12(1):e0169335. doi: 10.1371/journal.pone.0169335. eCollection 2017.

DOI:10.1371/journal.pone.0169335
PMID:28052097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5215656/
Abstract

Digestive cancers are major causes of mortality and morbidity worldwide. Fisetin, a naturally occurring flavonoid, has been previously shown anti-proliferative, anti-cancer, neuroprotective, and antioxidant activities. In our study, the anti-tumor activities in addition to regulatory effects of fisetin on some cancer cell lines were investigated. Data presented here showed that fisetin induces growth inhibition, and apoptosis in hepatic (HepG-2), colorectal (Caco-2) and pancreatic (Suit-2) cancer cell lines. Gene expression results showed that 1307 genes were significantly regulated in their expression in hepatic and pancreatic cell lines. 350 genes were commonly up-regulated and 353 genes were commonly down-regulated. Additionally, 604 genes were oppositely expressed in both tumor cells. CDK5 signaling, NRF2-mediated oxidative stress response, glucocorticoid signaling, and ERK/MAPK signaling were among most prominent signaling pathways modulating the growth inhibitory effects of fisetin on hepatic and pancreatic cancer cells. The present analysis showed, for the first time, that the anti-tumor effect of fisetin was mediated mainly through modulation of multiple signaling pathways and via activation of CDKN1A, SEMA3E, GADD45B and GADD45A and down-regulation of TOP2A, KIF20A, CCNB2 and CCNB1 genes.

摘要

消化系统癌症是全球范围内导致死亡和发病的主要原因。漆黄素是一种天然存在的类黄酮，此前已显示出具有抗增殖、抗癌、神经保护和抗氧化活性。在我们的研究中，除了研究漆黄素对某些癌细胞系的调节作用外，还对其抗肿瘤活性进行了研究。此处呈现的数据表明，漆黄素可诱导肝癌（HepG-2）、结直肠癌（Caco-2）和胰腺癌（Suit-2）细胞系的生长抑制和凋亡。基因表达结果显示，在肝癌和胰腺癌细胞系中，有1307个基因的表达受到显著调控。其中350个基因普遍上调，353个基因普遍下调。此外，在两种肿瘤细胞中，有604个基因的表达相反。CDK5信号通路、NRF2介导的氧化应激反应、糖皮质激素信号通路以及ERK/MAPK信号通路是调节漆黄素对肝癌和胰腺癌细胞生长抑制作用的最主要信号通路。本分析首次表明，漆黄素的抗肿瘤作用主要是通过调节多种信号通路以及激活CDKN1A、SEMA3E、GADD45B和GADD45A基因，并下调TOP2A、KIF20A、CCNB2和CCNB1基因来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c5/5215656/96abd6826640/pone.0169335.g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c5/5215656/96abd6826640/pone.0169335.g008.jpg

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