Evidence map›Paper›PMID 37932814›Full record

ArticleCell & bioscience2023

METTL3-mediated m6A methylation regulates ovarian cancer progression by recruiting myeloid-derived suppressor cells.

Jinyong Wang, Dakai Ling, Lulin Shi, Huayun Li, Minhua Peng, Huihong Wen, Tao Liu, Ruifang Liang, Yongjian Lin, Laiyou Wei and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. mFrontiers in immunology · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. MJournal of ovarian research · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. Epigenetic regulation in gynecological cancers: a paradigm shift in immunotherapy strategies.Journal of experimental & clinical cancer research : CR · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Enhancing mHeliyon · 2024
    Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 8 institutions in 2 countries.

Jinyong Wang *Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong, 518020, China.
Dakai Ling *Shenzhen International Institute for Biomedical Research, 518110, Shenzhen, Guangdong, China.
Lulin ShiDepartment of Hepatobiliary and Pancreas Surgery, Shenzhen People's Hospital, Shenzhen, Guangdong, 518020, China.
Huayun LiAnnoroad Gene Technology Corporation, Beijing, 100176, China.
Minhua PengShenzhen International Institute for Biomedical Research, 518110, Shenzhen, Guangdong, China.
Huihong WenShenzhen International Institute for Biomedical Research, 518110, Shenzhen, Guangdong, China.
Tao LiuAnnoroad Gene Technology Corporation, Beijing, 100176, China.
Ruifang LiangDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong, 518020, China.
Yongjian LinDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong, 518020, China.
Laiyou WeiDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong, 518020, China.
Guangzhi ZhangInstitute of Animal Sciences of Chinese Academy of Agriculture Sciences, Beijing, 100193, China. zgz_126com@126.com.
Shanze ChenDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong, 518020, China. chenshanze@mail.sustech.edu.cn.
Southern University of Science and Technology · CNAnnoroad Gene Technology (China) · CNGuangzhou Medical University · CNInstitute of Animal Sciences · CNJinan University · CNShenzhen Bay Laboratory · CNShenZhen People’s Hospital · CNWestern University · CA

Funding

National Natural Science Foundation of China 32100734National Natural Science Foundation of China 32100914Natural Science Foundation of Guangdong Province 2021A1515010478Natural Science Foundation of Guangdong Province 2214050008970
6 · The paper itself

Abstract

backgroundOvarian cancer (OC) typically develops an immunosuppressive microenvironment by funtional changes of host immune cells. Dysregulated m6A level is associated with cancer progression via the intrinsic oncogenic pathways. However, the role of m6A in regulating host immune cell function during anti-tumor immunity needs comprehensive analysis. This study aimed to investigate the role of METTL3, a catalytic subunit of the methyltransferase complex, in regulating host immune cell response against OC.

methodsIn this study, myeloid-specific Mettl3 gene knockout (Mettl3-cKO) mice were bred using the Cre-LoxP system. Intraperitoneally injection of ID8 cells was used as a syngeneic OC model. Furthermore, the compositions of immune cell populations were analyzed by flow cytometry and single-cell sequencing. Moreover, chemokines and cytokines secretion were assessed using ELISA. Lastly, the role of METTL3 in regulating IL-1β secretion and inflammasome activation in bone marrow-derived macrophages cocultured with ID8 cells was specified by ELISA and immunoblotting.

resultsIt was revealed that OC cell growth was enhanced in Mettl3-cKO mice. Furthermore, a shift of decreased M1 to increased M2 macrophage polarization was observed during OC progression. Moreover, Mettl3 depletion in myeloid lineage cells increased secretion of CCL2 and CXCL2 in peritoneal lavage fluild. Interestingly, Mettl3 deficiency enhanced IL-1β secretion induced by viable ID8 cells independent of inflammasome activation and cell death. Therefore, OC cells in tumor-bearing mice trigger a slight inflammatory response with a low-to-moderate secretion of pro-inflammatory cytokines and chemokines.

conclusionThis study provides new insights into METTL3-mediated m6A methylation, which regulates host immune response against OC.

Indexed as

Inflammatory responsesm6AMETTL3Myeloid-derived suppressive cellsOvarian cancerTumor microenvironment

Identifiers

PMID37932814
PMCPMC10629157
OpenAlexW4388424213

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.