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Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663
Shengshu Li1, Xiaoxin Lu2, Dongyang Zheng3
1Department of Pulmonary and Critical Care Medicine, The 8th Medical Center of Chinese, PLA General Hospital, Beijing, 100091, China.
Journal of Cancer Research and Clinical Oncology
|July 30, 2022
Summary
Methyltransferase-like protein 3 (METTL3) promotes lung cancer (LC) by enhancing m6A methylation of pri-miR-663, leading to increased cell proliferation and tumor growth. This study elucidates the METTL3-miR-663-SOCS6 pathway in LC progression.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Lung cancer (LC) is a significant global health concern.
- Methyltransferase-like protein 3 (METTL3) plays a role in cancer development through microRNA (miRNA) m6A modification.
Purpose of the Study:
- To investigate the role of METTL3 in LC progression.
- To determine how METTL3 affects m6A methylation-mediated processing of pri-miR-663 in LC.
Main Methods:
- RT-qPCR, CCK-8, Transwell, EdU, and flow cytometry assays were used to assess miR-663 expression and its effects on LC cell behavior.
- Dual-luciferase assays validated miR-663 targets.
- Co-immunoprecipitation and Me-RIP assays confirmed METTL3-DGCR8 interaction and m6A modification of pri-miR-663.
- In vivo tumor xenograft models evaluated METTL3's effect on tumor growth.
Main Results:
- miR-663 was upregulated in LC cells and promoted proliferation, migration, and invasion while inhibiting apoptosis.
- METTL3 interacted with DGCR8, and its silencing increased pri-miR-663 levels and m6A modification, suppressing miR-663 maturation.
- METTL3 facilitated tumor growth in mice via the miR-663/SOCS6 pathway, with miR-663 repressing SOCS6.
Conclusions:
- METTL3 promotes LC progression.
- This promotion occurs through accelerated m6A methylation-mediated pri-miR-663 processing.
- METTL3 also contributes to LC progression by repressing SOCS6 expression.
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