Open Access

Nature Communications

, volume 11 , issue 1 , publication number 2578

N6-methyladenosine regulates glycolysis of cancer cells through PDK4

Zihan Li ^{1, 2}

Yanxi Peng ^{1, 3}

Jiexin Li ¹

Zhuojia Chen ⁴

Feng Chen ¹

Jian Tu ²

Shuibin Lin ⁵

Hong Sheng Wang ¹

Hide authors affiliations Show authors affiliations: 5 affiliations

Guangdong Key Laboratory of Chiral Molecule and Drug Discovery, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China |

Institute of Pharmacy & Pharmacology, University of South China, Hengyang, China |

Department of Basic Medicine, Xiangnan University, Chenzhou, China |

⁴

Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China |

⁵

Center for Translational Medicine, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China |

Publication type: Journal Article

Publication date: 2020-05-22

Springer Nature

Nature Communications

scimago Q1

wos Q1

SJR: 4.761

CiteScore: 23.4

Impact factor: 15.7

ISSN: 20411723

DOI: 10.1038/s41467-020-16306-5

Copy DOI

PubMed ID: 32444598

General Chemistry

General Biochemistry, Genetics and Molecular Biology

General Physics and Astronomy

Abstract

Studies on biological functions of N6-methyladenosine (m6A) modification in mRNA have sprung up in recent years. We find m6A can positively regulate the glycolysis of cancer cells. Specifically, m6A-sequencing and functional studies confirm that pyruvate dehydrogenase kinase 4 (PDK4) is involved in m6A regulated glycolysis and ATP generation. The m6A modified 5′UTR of PDK4 positively regulates its translation elongation and mRNA stability via binding with YTHDF1/eEF-2 complex and IGF2BP3, respectively. Targeted specific demethylation of PDK4 m6A by dm6ACRISPR system can significantly decrease the expression of PDK4 and glycolysis of cancer cells. Further, TATA-binding protein (TBP) can transcriptionally increase the expression of Mettl3 in cervical cancer cells via binding to its promoter. In vivo and clinical data confirm the positive roles of m6A/PDK4 in tumor growth and progression of cervical and liver cancer. Our study reveals that m6A regulates glycolysis of cancer cells through PDK4. Dysregulation of N6-Methyladenosine (m6A) is associated with cancer progression. Here, authors show that m6A methylation of pyruvate dehydrogenase kinase 4 (PDK4) positively regulates its mRNA stability and translation, and consequently affects glycolysis in cancer cells

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Furuta Saori

40 publications, 1 169 citations, 125 reviews

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GOST Copy

Li Z. et al. N6-methyladenosine regulates glycolysis of cancer cells through PDK4 // Nature Communications. 2020. Vol. 11. No. 1. 2578

GOST all authors (up to 50) Copy

Li Z., Peng Y., Li J., Chen Z., Chen F., Tu J., Lin S., Wang H. S. N6-methyladenosine regulates glycolysis of cancer cells through PDK4 // Nature Communications. 2020. Vol. 11. No. 1. 2578

RIS |

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RIS Copy

TY - JOUR

DO - 10.1038/s41467-020-16306-5

UR - https://doi.org/10.1038/s41467-020-16306-5

TI - N6-methyladenosine regulates glycolysis of cancer cells through PDK4

T2 - Nature Communications

AU - Li, Zihan

AU - Peng, Yanxi

AU - Li, Jiexin

AU - Chen, Zhuojia

AU - Chen, Feng

AU - Tu, Jian

AU - Lin, Shuibin

AU - Wang, Hong Sheng

PY - 2020

DA - 2020/05/22

PB - Springer Nature

IS - 1

VL - 11

PMID - 32444598

SN - 2041-1723

ER -

BibTex

Cite this

BibTex (up to 50 authors) Copy

@article{2020_Li,

author = {Zihan Li and Yanxi Peng and Jiexin Li and Zhuojia Chen and Feng Chen and Jian Tu and Shuibin Lin and Hong Sheng Wang},

title = {N6-methyladenosine regulates glycolysis of cancer cells through PDK4},

journal = {Nature Communications},

year = {2020},

volume = {11},

publisher = {Springer Nature},

month = {may},

url = {https://doi.org/10.1038/s41467-020-16306-5},

number = {1},

pages = {2578},

doi = {10.1038/s41467-020-16306-5}

}

Publisher

Springer Nature

Journal

Nature Communications

scimago Q1

wos Q1

SJR

4.761

CiteScore

23.4

Impact factor

15.7

ISSN

20411723 (Print, Electronic)