Antrodia cinnamomea fruiting bodies extract suppresses the invasive potential of human liver cancer cell line PLC/PRF/5 through inhibition of nuclear factor kB pathway

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Title:	Antrodia cinnamomea fruiting bodies extract suppresses the invasive potential of human liver cancer cell line PLC/PRF/5 through inhibition of nuclear factor kB pathway 樟芝子實體萃取透物過抑制 NF-kB 路徑降低人類肝癌細胞株PLC/PRF/5 腫瘤入侵作用
Authors:	Wen-Chiu Ni(倪雯秋) Po-Lin Kuo(郭柏麟) Tz-Fei Tzeng(曾姿斐) Chien-Yu Cho(卓建宇) Ya-Ling Hsu(許雅玲) Chun-Ching Lin(林俊清)
Contributors:	Cell Biology Laboratory, Department of Biotechnology, Chia-Nan University of Pharmacy and Science Graduate lnstitute of Natural Products, Faculty of Pharmacy, College of Pharmacy, Kaohsiung Medical University
Date:	2008-07
Issue Date:	2017-12-04 16:00:59 (UTC+8)
Abstract:	Background and Purpose: Tumor invasiveness and metastasis are characteristics of highly malignant cancers with poor clinical outcome. Tumor invasion is a perplexing cascade process involving a finely tuned interaction between cancer cells and various regulated factors. In this study, we first report the anti-invasive effect of ethylacetate extract from Antrodia cinnamomea (EAC) fruiting bodies in the human liver cancer cell line PLC/PRF/5. Methods: Cell invasion assay. Electrophoretic mobility shift assay (EMSA) NF-κB reporter assay. MMP-2,MMP-9, and VEGF assay. Gelatin zymography. Western blot analysis. Matrigel plug angiogenesis assay. In vivo tumor model. Results: Treatment with EAC decreased the cancer invasion of PLC/PRF/5 cells in a dose-dependent manner. This effect was strongly associated with a concomitant decrease in either the level or activity of VEGF,MMP-2,MMP-9 and MT1-MMP, and an increase in the expression of TIMP-1 and TIMP-2. EAC inhibited constitutively activated and inducible NF-κB in both its DNA-binding activity and transcriptional activity. Furthermore, EAC also inhibited the TNF-α-activated NF-κB –dependent reporter gene expression of MMP-9 and VEGF, and the invasion of cancer cells. EAC also exhibited an inhibitory effect on angiogenesis in a Matrigel Plug Angiogenesis Assay. Further investigation revealed that EAC’s inhibition of cancer cell growth and invasion was also evident in a nude mice model. Our results indicate that EAC inhibits the activation of NF-κB, and may provide a molecular basis for drug development using EAC as an anti-invasive agent in the prevention and treatment of cancer. Conclusions: We have provided evidence demonstrating that EAC inhibits invasion and both MMPs and VEGF protein expression and enzyme activity. EAC suppresses invasion of PLC/PRF/5 cells by inhibition of NF-κB activity and sequentially reducing the expression and activity of MMP-9 in the cells. Therefore, we suggest that EAC could be potentially explored as a useful antiinvasive agent in the treatment of human liver carcinoma.
Relation:	第五屆海峽化學、生物及材料研討會，起迄日：2008/07/21-2008/07/22，地點：嘉南藥理科技大學
Appears in Collections:	[Dept. of Biotechnology (including master's program)] Proceedings [Pharmacy and Science] The 5rh Conference of Channel-bridge Chemistry, Biology and materal Science

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