Evidence map›Paper›PMID 35145841›Full record

ArticleJournal of bone oncology2022

m6A-dependent upregulation of TRAF6 by METTL3 is associated with metastatic osteosarcoma.

Jing Wang, Wentao Wang, Xing Huang, Jiashi Cao, Shuming Hou, Xiangzhi Ni, Cheng Peng, Tielong Liu

Abstract read
In one paragraph

Article in Journal of bone oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025
    Review
  5. METTL3-mediated SNHG1 mFrontiers in oncology · 2025
    Article
  6. mBiomaterials translational · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. The essential roles of mGenes & diseases · 2024
    Review
  11. Review
  12. Article
  13. Review
  14. Article
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

8 authors.

Jing WangDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Wentao WangDepartment of Orthopedics, Shanghai Changhai Hospital, Naval Medical University, Shanghai 200433, PR China.
Xing HuangDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Jiashi CaoDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Shuming HouDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Xiangzhi NiDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Cheng PengDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.
Tielong LiuDepartment of Orthopaedic Oncology, Spinal Tumor Center, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200003, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRNA N6-methyladenosine (m6A) is associated with tumorigenesis. The importance of methyltransferase-like 3 (METTL3) has been reported in cancer progression and metastasis. However, its role and molecular mechanism in osteosarcoma (OS), the most common primary bone tumor, is poorly studied. In this study, we aimed to investigate the functional role and underlying mechanism of METTL3 in the metastasis of OS.

methodsThe expression differences of METTL3 between metastatic and non-metastatic OS tissues and patients with different Enneking stages were detected using RT-qPCR. METTL3 was artificially downregulated in the cells, followed by wound healing assay, Matrigel assay, immunofluorescence,

resultsMETTL3 was overexpressed in metastatic OS tissues, and downregulation of METTL3 decreased cell migration, invasion, epithelial-mesenchymal transition, and tumorigenic and metastatic activities. The m6A site was highly enriched in cells poorly expressing METTL3, and the m6A peak was mainly enriched in the exon region. METTL3 was positively correlated with TRAF6 in metastatic OS, and depletion of METTL3 resulted in the loss of TRAF6 expression in OS cells. Upregulation of TRAF6 contributed to metastases

conclusionMETTL3 is highly expressed in OS and enhances TRAF6 expression through m6A modification, thereby promoting the metastases of OS cells.

Indexed as

m6AMetastasesMETTL3OsteosarcomaTRAF6

Identifiers

PMID35145841
PMCPMC8802048

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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.