METTL3 Promotes m6A-Dependent Maturation of pri-miR-150 to Regulate Proliferation of Esophageal Squamous Cell Carcinoma
10.3971/j.issn.1000-8578.2026.26.0167
- VernacularTitle:METTL3通过m6A甲基化促进pri-miR-150成熟调控食管鳞状细胞癌增殖
- Author:
Leilei SONG
1
;
Jingjing ZHANG
1
;
Hui WU
1
;
Zeyu XU
1
Author Information
1. Department of Clinical Laboratory, Huai'an 82 Hospital, Huai'an 223001, China.
- Publication Type:BASICRESEARCH
- Keywords:
Esophageal squamous cell carcinoma;
METTL3;
m6A;
pri-miR-150;
miR-150;
MYB
- From:
Cancer Research on Prevention and Treatment
2026;53(10):766-773
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the regulatory mechanism of methyltransferase like protein 3 (METTL3)–mediated m6A methylation in promoting pri-microRNA 150 (miR-150) maturation in esophageal squamous cell carcinoma (ESCC). Methods Quantitative real-time PCR and Western blot analysis were used to detect the expression of METTL3, pri-miR-150, miR-150, and MYB in ESCC cell lines, and lentiviral transfection and cell proliferation assays were applied to explore the role of METTL3 in ESCC cell proliferation. RNA immunoprecipitation and co-immunoprecipitation assays were used to confirm that METTL3 binds DGCR8 and regulates pri-miR-150 processing and maturation in an m6A methylation–dependent manner. Luciferase reporter assays were utilized to map the direct binding sites between miR-150 and MYB. Colony formation and CCK-8 assays confirmed that miR-150 functions in METTL3-induced ESCC cell proliferation. Results METTL3 expression was substantially upregulated in ESCC tissues and corresponding cell lines. ESCC cell proliferation was suppressed by METTL3 knockdown or enhanced by METTL3 overexpression. METTL3 mediates miR-150 processing and maturation via DGCR8, and miR-150 rescues METTL3-induced ESCC cell proliferation by targeting the MYB transcription factor. Conclusion This study demonstrates that METTL3 promotes pri-miR-150 processing and maturation in an m6A methylation–dependent manner by interacting with DGCR8, thereby enhancing ESCC cell proliferation and providing novel insights into ESCC diagnosis and treatment.
