Evidence map›Paper›PMID 37688756›Full record

ArticleGenes & genomics2023

m6A-mediated lncRNA NEAT1 plays an oncogenic role in non-small cell lung cancer by upregulating the HMGA1 expression through binding miR-361-3p.

Li Qi, Yue Yin, Mengqi Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024
    Review
  11. Article
  12. 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

3 authors at 2 institutions in 1 country.

Li QiDepartment of Oncology and Radiotherapy, The Second Affiliated Hospital of Harbin Medical University, No.246 Xuefu Road, Nangang District, Harbin, 150001, China. H05133@hrbmu.edu.cn.ORCID 0009-0009-9773-9162
Yue YinDepartment of Oncology and Radiotherapy, The Second Affiliated Hospital of Harbin Medical University, No.246 Xuefu Road, Nangang District, Harbin, 150001, China.
Mengqi SunDepartment of Oncology and Radiotherapy, Shenzhen People's Hospital, Shenzhen, 518020, China.
Harbin Medical University · CNShenZhen People’s Hospital · CN

Funding

Beijing Health Promotion Association Beijing Health Promotion Association
6 · The paper itself

Abstract

backgroundLung cancer is the most common primary malignant tumor of the lung, and 85% of lung cancer is non-small cell lung cancer (NSCLC). The N6-methyladenosine (m6A) and long noncoding RNAs (lncRNAs) have been widely reported to participate in the development of non-small cell lung cancer.

objectiveHowever, the potential molecular mechanisms of m6A-regulated lncRNAs in NSCLC still need further investigation.

methodsThe expression levels and the role of lncRNA NEAT1 in NSCLC tissues or cells were measured by RT-qPCR, Western blot, cell counting kit 8 (CCK-8), flow cytometry assay. RNA immunoprecipitation (RIP) was used to measure the levels of m6A modification of NEAT1. Bioinformatics analysis and dual-luciferase reporter gene assay were detected the relationship between miR-361-3p and NEAT1/HMGA1. Mouse xenograft tumor models were established to confirm the effects of lncRNA NEAT1 in vivo.

resultsIn this study, we verified whether m6A-modified lncRNA nuclear enriched abundant transcript 1 (NEAT1) is involved in NSCLC progression via miR-361-3p/HMGA1 axis. Firstly, we found that lncRNA NEAT1 was upregulated in NSCLC, and was associated with a poor survival in NSCLC patients. Methyltransferase like 3 (METTL3)-mediated m6A modification stabilized and upregulated NEAT1 expression. Next, function experiment indicated that depletion of METTL3 and NEAT1 induced cell apoptosis and inhibited cell proliferation, epithelial-mesenchymal transition (EMT). Likewise, in vivo experiments further supported the oncogenic role of NEAT1 in NSCLC. In addition, the molecular mechanism was uncovered in our study, and we found that lncRNA NEAT1 promoted the expression of high-mobility group AT-hook 1 (HMGA1) by sponging miR-361-3p and then promoted tumorigenesis of NSCLC.

conclusionIn conclusion, our findings demonstrated that METTL3-mediated m6A modification accelerated NSCLC progression by regulating the NEAT1/miR-361-3p/HMGA1 axis, which provides important targets for the treatment of NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsCell Line, TumorHMGA1a ProteinHumansMethyltransferasesMiceTranscription FactorsHMGA1a ProteinMethyltransferasesMETTL3 protein, humanMicroRNAsMIRN361 microRNA, humanRNA, Long NoncodingTranscription FactorsMethyltransferase like 3N6-methyladenosineNon-small cell lung cancerNuclear enriched abundant transcript 1

Identifiers

PMID37688756
OpenAlexW4386580057

What OpenQuestion holds

Textmetadata
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.