m6A-modified circRNA MYO1C participates in the tumor immune surveillance of pancreatic ductal adenocarcinoma through m6A/PD-L1 manner

Emerging evidence indicates the critical roles of N 6 -methyladenosine (m 6 A) modification in human cancers. Herein, our work reported that a novel m 6 A-modified circRNA from the MYO1C gene, circMYO1C, upregulated in the pancreatic ductal adenocarcinoma (PDAC). Our findings demonstrated that circM...

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Bibliographic Details
Published in:Cell death & disease 2023-02, Vol.14 (2), p.120-120, Article 120
Main Authors: Guan, Hua, Tian, Kun, Luo, Wei, Li, Mingfei
Format: Article
Language:English
Subjects:
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Adenocarcinoma
Antibodies
Biochemistry
Biomedical and Life Sciences
Biosynthesis
Cell Biology
Cell Culture
Cell migration
Cell proliferation
Cells
Epigenetics
Immunology
Immunoprecipitation
Immunosurveillance
Life Sciences
Mortality
mRNA stability
N6-methyladenosine
Pancreas
Pancreatic cancer
PD-L1 protein
Plasmids
RNA modification
Science
Tumorigenesis
Wound healing
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Summary:Emerging evidence indicates the critical roles of N 6 -methyladenosine (m 6 A) modification in human cancers. Herein, our work reported that a novel m 6 A-modified circRNA from the MYO1C gene, circMYO1C, upregulated in the pancreatic ductal adenocarcinoma (PDAC). Our findings demonstrated that circMYO1C is highly expressed in PDAC tissues. Functionally, circMYO1C promoted the proliferation and migration of PDAC cells in vitro and its silencing reduced the tumor growth in vivo. Mechanistically, circMYO1C cyclization was mediated by m 6 A methyltransferase METTL3. Moreover, methylated RNA immunoprecipitation sequencing (MeRIP-seq) unveiled the remarkable m 6 A modification on PD-L1 mRNA. Moreover, circMYO1C targeted the m 6 A site of PD-L1 mRNA to enhance its stability by cooperating with IGF2BP2, thereby accelerating PDAC immune escape. In conclusion, these findings highlight the oncogenic role of METTL3-induced circMYO1C in PDAC tumorigenesis via an m 6 A-dependent manner, inspiring a novel strategy to explore PDAC epigenetic therapy.
ISSN:2041-4889
2041-4889
DOI:10.1038/s41419-023-05570-0