中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
METTL3-induced UCK2 m(6)A hypermethylation promotes melanoma cancer cell metastasis via the WNT/beta-catenin pathway

文献类型:期刊论文

作者Wu, Hao1,2; Xu, Haochao1,2; Jia, Dongdong1,2; Li, Tao1,2; Xia, Liming1,2
刊名ANNALS OF TRANSLATIONAL MEDICINE
出版日期2021-07-13
ISSN号2305-5839
关键词Uridine-cytidine kinase 2 (UCK2) database m(6)A metastasis melanoma cancer
DOI10.21037/atm-21-2906
通讯作者Xia, Liming(doctorxlm@sina.com)
英文摘要Background: Melanoma is a highly aggressive, malignant skin tumor with a statistically high mortality rate. N6-methyladenosine (m(6)A) modification is involved in a variety of biological processes, including tumorigenesis. m(6)A modifications regulate the fate and functions of RNA, such as mRNA stability, nuclear processing, transport, localization, translation, primary microRNA (miRNA) processing, and RNA-protein interactions. Several members (including METTL3, METTL14, FTO, ALKBH5, and YTHDF2) are actively involved in a variety of human cancers. However, the basic mechanism of the involvement of uridine cytidine kinase 2 (UCK2) in melanoma metastasis has not been studied. UCK2 is upregulated in a variety of malignancies. However, the complex molecular mechanisms and therapeutic effects of UCK2 in melanoma remain unclear. Methods: The expression of UCK2 was evaluated by qRT-PCR. The effects of UCK2 on the biological characteristics of PC cells were investigated on the basis of loss-of-function analyses. ImmunoprecipitationqPCR (MeRIP-qPCR) was performed to identify the m(6)A targeted effect of UCK2 in melanoma cancer. Results: Based on the bioinformatics analysis in this study, up-regulation of UCK2 could be essential in melanoma cancer, and associated with poor survival. Furthermore, the m(6)A modification regulated by METTL3 led to UCK2 increased messenger RNA (mRNA) stability in melanoma cancer. Functional and mechanistic experiments indicated that UCK2 enhanced the metastasis of melanoma cancer cells through the WNT/13-catenin pathway. Conclusion: In this study, we found that m(6)A-METTL3 axis induced abnormal UCK2 expression plays a role in melanoma metastasis by enhancing the Wnt/13-catenin pathway, which may provide new clues for melanoma metastasis. It also provides a potential target for the prevention and treatment of melanoma.
WOS关键词CYTIDINE KINASE 2 ; PROLIFERATION ; STATISTICS ; ACTIVATION ; EXPRESSION ; BIOMARKER ; INVASION ; ASSAY
资助项目Health Science and Technology program of Zhejiang Province[2021KY106]
WOS研究方向Oncology ; Research & Experimental Medicine
语种英语
出版者AME PUBL CO
WOS记录号WOS:000677657200001
资助机构Health Science and Technology program of Zhejiang Province
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/123200]  
专题中国科学院合肥物质科学研究院
通讯作者Xia, Liming
作者单位1.Univ Chinese Acad Sci, Canc Hosp, Dept Bone & Soft Tissue Surg, Zhejiang Canc Hosp, Hangzhou, Peoples R China
2.Chinese Acad Sci, Inst Canc & Basic Med IBMC, Hangzhou, Peoples R China
推荐引用方式
GB/T 7714
Wu, Hao,Xu, Haochao,Jia, Dongdong,et al. METTL3-induced UCK2 m(6)A hypermethylation promotes melanoma cancer cell metastasis via the WNT/beta-catenin pathway[J]. ANNALS OF TRANSLATIONAL MEDICINE,2021.
APA Wu, Hao,Xu, Haochao,Jia, Dongdong,Li, Tao,&Xia, Liming.(2021).METTL3-induced UCK2 m(6)A hypermethylation promotes melanoma cancer cell metastasis via the WNT/beta-catenin pathway.ANNALS OF TRANSLATIONAL MEDICINE.
MLA Wu, Hao,et al."METTL3-induced UCK2 m(6)A hypermethylation promotes melanoma cancer cell metastasis via the WNT/beta-catenin pathway".ANNALS OF TRANSLATIONAL MEDICINE (2021).

入库方式: OAI收割

来源:合肥物质科学研究院

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