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m6A甲基转移酶METTL3通过调节TCF1上的m6A甲基化促进甲状腺癌进展。

Progression of Thyroid Carcinoma Is Promoted by the m6A Methyltransferase METTL3 Through Regulating mA Methylation on TCF1.

作者信息

Wang Kejin, Jiang Lin, Zhang Yan, Chen Chao

机构信息

Department of Head and Neck Surgery, Cancer Hospital of University of Chinese Academy of Sciences, Key Laboratory of Head & Neck Cancer Translational Research of Zhejiang Province, Hangzhou, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Feb 21;13:1605-1612. doi: 10.2147/OTT.S234751. eCollection 2020.

DOI:10.2147/OTT.S234751
PMID:32158230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7044742/
Abstract

OBJECTIVE

This study aims to uncover the progression of thyroid carcinoma influenced by the m6A methyltransferase METTL3 through regulating mA methylation on TCF1 mRNA and the activated Wnt pathway.

METHODS

Thyroid carcinoma tissues and paracancerous ones were collected for detecting levels of METTL3 and TCF1. Potential correlation between levels of METTL3 and TCF1 was analyzed by Pearson analysis. Survival of thyroid carcinoma patients influenced by METTL3 level was assessed by Kaplan-Meier method. Regulatory effect of METTL3 on migratory ability in TPC-1 cells was examined by wound healing assay. The interaction between METTL3 with TCF1 and IGF2BP2 was verified by RNA-Binding Protein Immunoprecipitation (RIP) assay. Meanwhile, the activity of the Wnt pathway was reflected by TOP/FOP-Flash. At last, rescue experiments were conducted to clarify the involvement of TCF1 in phenotype changes of thyroid carcinoma cells that were regulated by METTL3.

RESULTS

METTL3 and TCF1 were upregulated in thyroid carcinoma. Similarly, METTL3 was highly expressed in thyroid carcinoma cells as well. Kaplan-Meier method uncovered poor prognosis in thyroid carcinoma patients expressing a high level of METTL3. Silence of METTL3 inhibited migratory ability and Wnt activity in TPC-1 cells. RIP assay confirmed the interaction between TCF1 and METTL3 or IGF2BP2. Moreover, METTL3 positively regulated the enrichment abundance of TCF1 in anti-IGF2BP2. Rescue experiments demonstrated that TCF1 was responsible for METTL3-regulated thyroid carcinoma progression via the mA methylation.

CONCLUSION

Upregulated m6A methyltransferase METTL3 promotes the progression of thyroid carcinoma through mA methylation on TCF1.

摘要

目的

本研究旨在揭示m6A甲基转移酶METTL3通过调节TCF1 mRNA上的m6A甲基化和激活Wnt信号通路对甲状腺癌进展的影响。

方法

收集甲状腺癌组织和癌旁组织，检测METTL3和TCF1水平。采用Pearson分析方法分析METTL3和TCF1水平之间的潜在相关性。采用Kaplan-Meier法评估METTL3水平对甲状腺癌患者生存的影响。采用伤口愈合实验检测METTL3对TPC-1细胞迁移能力的调节作用。通过RNA结合蛋白免疫沉淀（RIP）实验验证METTL3与TCF1和IGF2BP2之间的相互作用。同时，通过TOP/FOP-Flash反映Wnt信号通路的活性。最后，进行挽救实验以阐明TCF1在METTL3调节的甲状腺癌细胞表型变化中的作用。

结果

甲状腺癌中METTL3和TCF1表达上调。同样，METTL3在甲状腺癌细胞中也高表达。Kaplan-Meier法显示，METTL3高表达的甲状腺癌患者预后较差。沉默METTL3可抑制TPC-1细胞的迁移能力和Wnt活性。RIP实验证实了TCF1与METTL3或IGF2BP2之间的相互作用。此外，METTL3正向调节抗IGF2BP2中TCF1的富集丰度。挽救实验表明，TCF1通过m6A甲基化参与了METTL3调节的甲状腺癌进展。

结论

上调的m6A甲基转移酶METTL3通过对TCF1进行m6A甲基化促进甲状腺癌进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/eb9e13389206/OTT-13-1605-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/f2b75bbc991b/OTT-13-1605-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/a497b62b0360/OTT-13-1605-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/7a40beb0e0fd/OTT-13-1605-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/eb9e13389206/OTT-13-1605-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/f2b75bbc991b/OTT-13-1605-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/a497b62b0360/OTT-13-1605-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/7a40beb0e0fd/OTT-13-1605-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7bc/7044742/eb9e13389206/OTT-13-1605-g0004.jpg

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