Baicalin hydrate inhibits cancer progression in nasopharyngeal carcinoma by affecting genome instability and splicing
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Weiwei Lai1,2, Jiantao Jia1,2,4, Bin Yan1,2, Yiqun Jiang1,2, Ying Shi1,2, Ling Chen1,2, Chao Mao1,2, Xiaoli Liu1,2, Haosheng Tang1,2,3, Menghui Gao1,2,3, Ya Cao1,2, Shuang Liu5 and Yongguang Tao1,2,3
1Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, China
2Cancer Research Institute, Central South University, Changsha, Hunan, China
3Department of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha, Hunan, China
4Changzhi Medical College, Changzhi, Shanxi, China
5Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan, China
Yongguang Tao, email: [email protected]
Keywords: baicalin hydrate; genome stability; splicing; DNA methylation; m6A RNA methylation
Received: April 19, 2017 Accepted: September 20, 2017 Published: December 04, 2017
Baicalin hydrate (BH), a natural compound, has been investigated for many years because of its traditional medicinal properties. However, the anti-tumor activities of BH and its epigenetic role in NPC have not been elucidated. In this study, we identified that BH inhibits NPC cell growth in vivo and in vitro by inducing apoptosis and cell cycle arrest. BH epigenetically regulated genome instability by up-regulating the expression of satellite 2 (Sat2), alpha satellite (α-Sat), and major satellite (Major-Sat). BH also increased the level of IKKα, Suv39H1, and H3K9me3 and decreased LSH expression. Interestingly, BH promoted the splicing of Suv39H1 via the enhancement of m6A RNA methylation, rather than DNA methylation. Taken together, our results demonstrated that BH has an anti-tumor role in NPC and revealed a unique role of BH in genome instability and splicing in response to DNA damage.
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