1. IE browser is NOT supported anymore. Please use Chrome, Firefox or Edge instead.
2. If you are a new user, please register to get an IHEP SSO account through https://login.ihep.ac.cn/registlight.jsp Any questions, please email us at helpdesk@ihep.ac.cn or call 88236855.
3. If you need to create a conference in the "Conferences, Workshops and Events" zone, please email us at helpdesk@ihep.ac.cn.
4. The max file size allowed for upload is 100 Mb.
26–28 Dec 2020
Asia/Shanghai timezone
2020金属组学研讨会暨北京金属组学平台年会及原子光谱沙龙年会顺利结束,期待再次相聚!

LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle Arrest through Destabilizing EZH2 and Facilitating NFATc2 Expression

Not scheduled
15m
墙报

Speaker

Dr Ming Gao (Research Center for Eco-Environmental Sciences Chinese Academy of Sciences)

Description

Arsenic (As) is a widespread metalloid contaminant, and its internal exposure is demonstrated to cause serious detrimental health problems. Albeit considerable studies are performed to interrogate the molecular mechanisms responsible for As-induced toxicities, the exact mechanisms are not fully understood yet, especially at the epigenetic regulation level. In the present study, it is identified that long non-coding RNA (lncRNA) urothelial cancer associated 1 (UCA1) alleviates As-induced G2/M phase arrest in human liver cells. Intensive mechanistic investigations illustrate that UCA1 interacts with enhancer of zeste homolog 2 (EZH2) and accelerates the latter’s protein turnover rate under normal and As-exposure conditions. The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2. As a consequence, the cell cycle regulator nuclear factor of activated T cells 2 (NFATc2), a downstream target of EZH2, is upregulated to resist As-blocked cell cycle progress and cytotoxicity. This current study unearths a novel prosurvival signaling pathway conducted by EZH2 under As-induced cell cycle arrest. In conclusion, Our present study obtains novel insights into the complex networks of defense mechanisms against As threat, and opens a new path to understand the deregulation of cell cycle progression under pollutant exposure. The findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.

Primary authors

Dr Ming Gao (Research Center for Eco-Environmental Sciences Chinese Academy of Sciences) Dr zheng Dong (Research Center for Eco-Environmental Sciences Chinese Academy of Sciences)

Co-authors

Dr Changying Li (Research Center for Eco-Environmental Sciences Chinese Academy of Sciences) Dr Min Cong (Liver Research Center Beijing Friendship Hospital) Dr Sijing Liu (Research Center for Eco-Environmental Sciences Chinese Academy of Sciences)

Presentation materials

There are no materials yet.