Evidence map›Paper›PMID 34842045›Full record

ArticleBioengineered2021

Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis.

Guoping Wang, Zhongchen Zhang, Chenmei Xia

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. The miR-338-5p/METTL3 axis regulates m6A modification to inhibit tumor progression in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
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  7. NJournal of translational internal medicine · 2024
    Article
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  9. New insights into the regulation of METTL3 and its role in tumors.Cell communication and signaling : CCS · 2023
    Review
  10. Review
  11. Novel insights into mutual regulation between NCancer cell international · 2023
    Review
  12. Emerging Mutual Regulatory Roles between mInternational journal of molecular sciences · 2023
    Review
  13. Review
  14. The emerging role of mFrontiers in cell and developmental biology · 2023
    Review
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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

3 authors at 1 institution in 1 country.

Guoping WangDepartment of Endoscopy Center, First People's Hospital of Wenling, Wenling, Zhejiang, China.
Zhongchen ZhangDepartment of Endoscopy Center, First People's Hospital of Wenling, Wenling, Zhejiang, China.
Chenmei XiaDepartment of Endoscopy Center, First People's Hospital of Wenling, Wenling, Zhejiang, China.ORCID 0000-0001-8871-3133
The First People's Hospital of Wenling · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a common cancer with high incidence. Understanding the epidemiology and physiopathology of GC is crucial for formulating novel therapeutic strategies. Recent studies have implicated long non-coding RNA LINC00240, miR-338-5p and methyltransferase-like 3 (METTL3) in the progression of GC. In this study, we investigated the functional role of LINC00240/miR-338-5p/METTL3 axis in regulating the aggressiveness of GC cells. We first demonstrated that LINC00240 was upregulated in GC tissues and GC cell lines. High expression of LINC00240 was associated with advanced TNM stage, a higher extent of distant metastasis and lymph nodes metastasis, and the poor overall and disease-free survival of the patients. In GC cell lines, the knockdown of LINC00240 inhibited GC cell proliferation and migration, but induced cell apoptosis. We further identified and validated the functional interaction between LINC00240 and miR-338-5p. miR-338-5p seemed to function as a downstream target negatively regulated by LINC00240, and miR-338-5p could target METTL3 at 3' UTR to downregulate its expression. In GC tissues, the expression of miR-338-5p was negatively correlated with LINC00240, and the expression of miR-338-5p was negatively correlated with METTL3. Importantly, miR-338-5p inhibitor or METTL3 overexpression could rescue the inhibitory effect of LINC00240 knockdown on cell proliferation and migration, and inhibit the apoptosis induction in GC cells. Taken together, our data imply that the upregulation of LINC00240 in GC cells promotes the malignant phenotype by modulating miR-338-5p/METTL3 axis, which could serve as potential therapeutic targets for GC treatment.

Indexed as

Signal TransductionCell Line, TumorCell MovementCell ProliferationHumansMethyltransferasesMicroRNAsNeoplasm ProteinsRNA, Long NoncodingRNA, NeoplasmStomach NeoplasmsMethyltransferasesMETTL3 protein, humanMicroRNAsMIRN338 microRNA, humanNeoplasm ProteinsRNA, Long NoncodingRNA, Neoplasmcell functiongastric cancerLINC00240METTL3miR-338-5p

Identifiers

PMID34842045
PMCPMC8810089
OpenAlexW3215212805

What Socratic holds

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LicenceCC BY
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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 Socratic graph.