NDLI: TQ inhibits hepatocellular carcinoma growth in vitro and in vivo via repression of Notch signaling

Content Provider	PubMed Central
Author	Ke, Xiquan Zhao, Yan Lu, Xinlan Wang, Zhe Liu, Yuanyuan Ren, Mudan Lu, Guifang Zhang, Dan Sun, Zhenguo Xu, Zhipeng Song, Jee Hoon Cheng, Yulan Meltzer, Stephen J. He, Shuixiang
Copyright Year	2015
Abstract	Thymoquinone (TQ) has been reported to possess anti-tumor activity in various types of cancer. However, its effects and molecular mechanism of action in hepatocellular carcinoma (HCC) are still not completely understood. We observed that TQ inhibited tumor cell growth in vitro, where treatment with TQ arrested the cell cycle in G1 by upregulating p21 and downregulating cyclinD1 and CDK2 expression; moreover, TQ induced apoptosis by decreasing expression of Bcl-2 and increasing expression of Bax. Simultaneously, TQ demonstrated a suppressive impact on the Notch pathway, where overexpression of NICD1 reversed the inhibitory effect of TQ on cell proliferation, thereby attenuating the repressive effects of TQ on the Notch pathway, cyclinD1, CDK2 and Bcl-2, and also diminishing upregulation of p21 and Bax. In a xenograft model, TQ inhibited HCC growth in nude mice; this inhibitory effect in vivo, as well as of HCC cell growth in vitro, was associated with a discernible decline in NICD1 and Bcl-2 levels and a dramatic rise in p21 expression. In conclusion, TQ inhibits HCC cell growth by inducing cell cycle arrest and apoptosis, achieving these effects by repression of the Notch signaling pathway, suggesting that TQ represents a potential preventive or therapeutic agent in HCC patients.
Related Links	http://dx.doi.org/10.18632/oncotarget.5362
Ending Page	32621
Page Count	12
Starting Page	32610
File Format	PDF
ISSN	19492553
e-ISSN	19492553
Journal	Oncotarget
Issue Number	32
Volume Number	6
Language	English
Publisher	Impact Journals LLC
Publisher Date	2015-10-01
Access Restriction	Open
Rights Holder	Impact Journals LLC
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Oncology

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