Evidence map›Paper›PMID 35925508›Full record

ArticleJournal of cell communication and signaling2023

METTL13 facilitates cell growth and metastasis in gastric cancer via an eEF1A/HN1L positive feedback circuit.

Qiong Wu, Qingqing Hu, Yanan Hai, Yandong Li, Yong Gao

Open access · hybridFull text read
In one paragraph

Article in Journal of cell communication and signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. METTL Family in Healthy and Disease.Molecular biomedicine · 2024
    Review
  13. Diagnostic and Prognostic Value of Methyltransferase Like 13 in Hepatocellular Carcinoma Based on Bioinformatics Analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 2 institutions in 1 country.

Qiong WuDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, 150 Ji-Mo Rd., Shanghai, 200120, China.ORCID http://orcid.org/0000-0002-7071-3773
Qingqing HuDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, 150 Ji-Mo Rd., Shanghai, 200120, China.
Yanan HaiDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, 150 Ji-Mo Rd., Shanghai, 200120, China.
Yandong LiDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, 150 Ji-Mo Rd., Shanghai, 200120, China. yandongli2009@gmail.com.
Yong GaoDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, 150 Ji-Mo Rd., Shanghai, 200120, China. drgaoyong@tongji.edu.cn.
Shanghai East Hospital · CNTongji University · CN

Funding

the National Natural Science Foundation of China No. 81772567the National Natural Science Foundation of China No. 81972290the Top-level Clinical Discipline Project of Shanghai Pudong No. PWYgf2021-07
6 · The paper itself

Abstract

Although improved treatment could inhibit progression of gastric cancer (GC), the recurrence and metastasis remain challenging issues. Methyltransferase like 13 (METTL13) has been implicated in most human cancers, but its function and mechanism in GC remain elusive. In the present study, we evaluated its expression in GC samples and found it was aberrantly overexpressed in cancer tissues than that in normal stomach tissues. High expression of METTL13 was closely associated with age, tumor size and T classification. Biological experiments showed that silencing METTL13 suppressed gastric cancer cell proliferation and metastasis in vivo and vitro, whereas opposite effects were observed upon METTL13 overexpression. Further mechanistic explorations revealed that METTL13 regulated the expression of HN1L (Hematological and neurological expressed 1-like), which is reported to be an oncogene in various cancers. Knockdown of HN1L dampened gastric cancer cell growth induced by METTL13. Eukaryotic translation elongation factor-1A (eEF1A), the present sole methylation substrate of METTL13, was involved in the regulation of HN1L by METTL13 in a K55 methylation independent manner. In addition, we also found HN1L could facilitate METTL13 expression in GC cells consistent with a previous report in hepatocellular carcinoma. Thus, these findings demonstrate a METTL13/eEF1A/HN1L positive feedback circuit promoting gastric cancer development and metastasis. It will help develop promising diagnostic and therapeutic targets for this disease.

Indexed as

eEF1AGastric cancerHN1LMetastasisMETTL13

Identifiers

PMID35925508
PMCPMC10030728
OpenAlexW4289745330

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read35
Read underepoch 390

Registered trials

None linked

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.