Journal
CELL DEATH & DISEASE
Volume 9, Issue -, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-018-1224-3
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Funding
- Youth Science and Technology Innovation Talent of Guangdong TeZhi Plan [2017TQ04R754]
- Natural Science Foundation of GuangDong Province [2017A030310227, 2017A030312003]
- open project of State Key Laboratory of Oncology in South China [HN2017-03]
- Health & Medical Collaborative Innovation Project of Guangzhou City, China [201803040003]
- Innovation Team Development Plan of the Ministry of Education [IRT_17R110]
- Overseas Expertise Introduction Project for Discipline Innovation (111 Project) [B14035]
- National Natural Science Foundation of China [81802920]
- Natural Science Funding of Shenzhen [JCYJ20160422091914681]
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Nasopharyngeal carcinoma (NPC) progression is regulated by genetic, epigenetic, and epitranscript modulation. As one of the epitranscript modifications, the role of N6-Methyladenosine (m(6)A) has not been elucidated in NPC. In the present study, we found that the poorly methylated gene ZNF750 (encoding zinc finger protein 750) was downregulated in NPC tumor tissues and cell lines. Ectopic expression of ZNF750 blocked NPC growth in vitro and in vivo. Further studies revealed that m(6)A modifications maintained the low expression level of ZNF750 in NPC. Chromatin immunoprecipitation sequencing identified that ZNF750 directly regulated FGF14 (encoding fibroblast growth factor 14), ablation of which reversed ZNF750's tumor repressor effect. Moreover, the ZNF750-FGF14 signaling axis inhibited NPC growth by promoting cell apoptosis. These findings uncovered the critical role of m(6)A in NPC, and stressed the regulatory function of the ZNF750-FGF14 signaling axis in modulating NPC progression, which provides theoretical guidance for the clinical treatment of NPC.
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