Evidence map›Paper›PMID 35348293›Full record

ArticleJournal of cellular and molecular medicine2022

METTL3-mediated maturation of miR-589-5p promotes the malignant development of liver cancer.

Jie Liu, Kai Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. 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
2.2field-weighted citation impact, top 12% 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, 25 citations in OpenAlex.

  1. Review
  2. METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Clinical significance of RNA methylation in hepatocellular carcinoma.Cell communication and signaling : CCS · 2024
    Review
  11. RNA m6A methylation regulators in liver cancer.Cancer cell international · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  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

2 authors at 1 institution in 1 country.

Jie LiuHepatobiliary and Pancreatic Surgery Department, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Kai JiangHepatobiliary and Pancreatic Surgery Department, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.ORCID 0000-0001-5935-1663
Zhejiang Provincial People's Hospital · CN

Funding

Natural Science Foundation of Zhejiang Province LY21H160050Zhejiang Medical and Health Department Project 2020KY044Zhejiang Traditional Chinese Medicine Science and Technology Project 2020ZA014
6 · The paper itself

Abstract

MiR-589-5p could promote liver cancer, but the specific mechanisms are largely unknown. This study examined the role and mechanisms of miR-589-5p in liver cancer. The expressions of miR-589-5p, METTL3 and m6A in liver cancers were determined by RT-qPCR. The relationship between miR-589-5p and METTL3-mediated m6A methylation was examined by m6A RNA immunoprecipitation. After transfection, the viability, migration, invasion and expressions of METTL3 and miR-589-5p in liver cancer cells were detected by CCK-8, wound-healing, transwell and RT-qPCR. After the xenograft tumour was established in mice, the tumour volume was determined and the expressions of METTL3, miR-589-5p, MMP-2, TIMP-2, E-cadherin, N-cadherin and Vimentin in tumour tissue were detected by RT-qPCR and Western blotting. In vitro study showed that miR-589-5p and METTL3 were highly expressed in liver cancer. METTL3 was positively correlated with miR-589-5p. METTL3 up-regulated the expression of miR-589-5p and promoted the maturation of miR-589-5p. Overexpressed miR-589-5p and METTL3 promoted the viability, migration and invasion of liver cancer cells, while the effects of silencing miR-589-5p and METTL3 on the cells were the opposite. The effects of METTL3 overexpression and silencing were reversed by miR-589-5p inhibitor and mimic, respectively. In vivo study showed that METLL3 silencing inhibited the growth of xenograft tumour and the expressions of METTL3, MMP-2, N-cadherin and Vimentin, promoted the expressions of TIMP-2 and E-cadherin, while miR-589-5p mimic caused the opposite results and further reversed the effects of METLL3 silencing. In summary, this study found that METTL3-mediated maturation of miR-589-5p promoted the malignant development of liver cancer.

Indexed as

Liver NeoplasmsMicroRNAsAnimalsCadherinsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMatrix Metalloproteinase 2MethyltransferasesMiceTissue Inhibitor of Metalloproteinase-2VimentinCadherinsMatrix Metalloproteinase 2MethyltransferasesMETTL3 protein, humanMettl3 protein, mouseMicroRNAsMIRN589 microRNA, humanTissue Inhibitor of Metalloproteinase-2Vimentinliver cancerm6A methylationMETTL3miR-589-5ppri-miR-589

Identifiers

PMID35348293
PMCPMC9077310
OpenAlexW4220990124

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.