Antrodia camphorata and coenzyme Q0, a novel quinone derivative of Antrodia camphorata, impede HIF-1α and epithelial-mesenchymal transition/metastasis in human glioblastoma cells

doi:10.1002/tox.23785

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Title:	Antrodia camphorata and coenzyme Q0, a novel quinone derivative of Antrodia camphorata, impede HIF-1α and epithelial-mesenchymal transition/metastasis in human glioblastoma cells
Authors:	Yang, Hsin-Ling Chang, Yao-Hsien Pandey, Sudhir Bhat, Asif Ali Vadivalagan, Chithravel Lin, Kai-Yuan Hseu, You-Cheng
Contributors:	China Med Univ, Inst Nutr, Coll Pharm China Med Univ, Coll Pharm, Dept Cosmeceut Chi Mei Med Ctr, Dept Med Res Chia Nan Univ Pharm & Sci, Dept Biotechnol Asia Univ, Dept Hlth & Nutr Biotechnol China Med Univ, Chinese Med Res Ctr China Med Univ, Res Ctr Chinese Herbal Med China Med Univ, Coll Pharm, Dept Cosmeceut
Keywords:	Antrodia camphorata autophagy CoQ(0) EMT/metastasis glioblastoma HIF-1 alpha
Date:	2023
Issue Date:	2024-12-25 11:05:37 (UTC+8)
Publisher:	WILEY
Abstract:	Antrodia camphorata (AC) and Coenzyme Q(0) (CoQ(0)), a novel quinone derivative of AC, exhibits antitumor activities. The present study evaluated EMT/metastasis inhibition and autophagy induction aspects of AC and CoQ(0) in human glioblastoma (GBM8401) cells. Our findings revealed that AC treatment (0-150 mu g/mL) hindered tumor cell proliferation and migration/invasion in GBM8401 cells. Notably, AC treatment inhibited HIF-1 alpha and EMT by upregulating epithelial marker protein E-cadherin while downregulating mesenchymal proteins Twist, Slug, Snail, and beta-catenin. There was an appearance of the autophagy markers LC3-II and p62/SQSTM1, while ATG4B was downregulated by AC treatment. We also found that CoQ(0) (0-10 mu M) could inhibit migration and invasion in GBM8401 cells. In particular, E-cadherin was elevated and N-cadherin, Vimentin, Twist, Slug, and Snail, were reduced upon CoQ(0) treatment. In addition, MMP-2/-9 expression and Wnt/beta-catenin pathways were downregulated. Furthermore, autophagy inhibitors 3-MA or CQ reversed the CoQ(0)-elicited suppression of migration/invasion and metastasis-related proteins (Vimentin, Snail, and beta-catenin). Results suggested autophagy-mediated antiEMT and antimetastasis upon CoQ(0) treatment. CoQ(0) inhibited HIF-1 alpha and metastasis in GBM8401 cells under normoxia and hypoxia. HIF-1 alpha knockdown using siRNA accelerated CoQ(0)-inhibited migration. Finally, CoQ(0) exhibited a prolonged survival rate in GBM8401-xenografted mice. Treatment with Antrodia camphorata/CoQ(0) inhibited HIF-1 alpha and EMT/metastasis in glioblastoma.
Relation:	Environmental Toxicology, v.38, n.7, pp.1548-1564
Appears in Collections:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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