Evidence map›Paper›PMID 34398984›Full record

ArticleJournal of clinical laboratory analysis2021

METTL3-mediated m6A methylation of ASPM drives hepatocellular carcinoma cells growth and metastasis.

An Wang, Xiaofeng Chen, Dongen Li, Liang Yang, Jianshuai Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Microtubule Minus-End Binding Proteins in Cancer: Advances.Diagnostics (Basel, Switzerland) · 2025
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  4. mMolecules (Basel, Switzerland) · 2025
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  5. Article
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  7. Article
  8. RNA m6A methylation regulators in liver cancer.Cancer cell international · 2024
    Review
  9. Review
  10. Article
  11. Recent Advances in RNA mCancer treatment and research · 2023
    Article
  12. Article
  13. Role of m6A writers, erasers and readers in cancer.Experimental hematology & oncology · 2022
    Review
  14. Article
  15. Article
  16. 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 1 institution in 1 country.

An WangDepartment of General Surgery, Ningbo First Hospital, Ningbo, China.
Xiaofeng ChenDepartment of General Surgery, Ningbo First Hospital, Ningbo, China.
Dongen LiDepartment of General Surgery, Ningbo First Hospital, Ningbo, China.
Liang YangDepartment of General Surgery, Ningbo First Hospital, Ningbo, China.
Jianshuai JiangDepartment of General Surgery, Ningbo First Hospital, Ningbo, China.ORCID https://orcid.org/0000-0002-8989-8528
Ningbo First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormal spindle-like microcephaly (ASPM) has been proved to participate in tumor progression. However, the underlying mechanism of ASPM in liver hepatocellular carcinoma (LIHC) remains elusive.

methodsThe mRNA and protein expression were determined using Western blot and qRT-PCR, and the capacities of cells proliferation, migration, and invasion were evaluated by CCK-8, colony formation, wound healing, and transwell. MeRIP was performed to validate the interaction between ASPM and methyltransferase-like 3 (METTL3).

resultsHerein, we found that ASPM was significantly upregulated in LIHC, and the high expression of ASPM was associated with poor LIHC prognosis. Furthermore, ASPM knockdown could suppress LIHC cells proliferation, migration, and invasion, while ASPM overexpression exerted reverse effect. Mechanistically, we revealed that the N6-methyladenosine (m6A) modification of ASPM mRNA mediated by METTL3 promoted its expression in LIHC. More importantly, silencing METTL3 suppressed LIHC cells proliferation, migration, and invasion, which could be retained by ASPM overexpression.

conclusionCollectively, our findings suggested that METTL3/ASPM axis could serve as a novel promising therapeutic candidate for LIHC.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticAdenosineApoptosisCarcinoma, HepatocellularCell MovementCell ProliferationDisease ProgressionHumansLiver NeoplasmsMethyltransferasesNerve Tissue ProteinsPrognosisSurvival RateTumor Cells, CulturedAdenosineASPM protein, humanMethyltransferasesMETTL3 protein, humanNerve Tissue ProteinsN-methyladenosineASPMcells proliferationhepatocellular carcinomainvasionLIHCm6Amigration

Identifiers

PMID34398984
PMCPMC8418466
OpenAlexW3194779127

What OpenQuestion holds

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LicenceCC BY-NC
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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.