Evidence map›Paper›PMID 35730068›Full record

ArticleCancer communications (London, England)2022

Gene amplification-driven RNA methyltransferase KIAA1429 promotes tumorigenesis by regulating BTG2 via m6A-YTHDF2-dependent in lung adenocarcinoma.

Chang Zhang, Qi Sun, Xu Zhang, Na Qin, Zhening Pu, Yayun Gu, Caiwang Yan, Meng Zhu, Juncheng Dai, Cheng Wang and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cancer communications (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. KIAA1429-mediated MCellular & molecular biology letters · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

17 authors at 5 institutions in 3 countries.

Chang ZhangDepartment of Epidemiology, School of Public Health, Southeast University, Nanjing, Jiangsu, 210009, P. R. China.
Qi SunDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Xu ZhangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Na QinDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Zhening PuCenter of Clinical Research, Wuxi People's Hospital of Nanjing Medical University, Wuxi, Jiangsu, 214023, P. R. China.
Yayun GuDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Caiwang YanDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Meng ZhuDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Juncheng DaiDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Cheng WangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Ni LiDepartment of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, P. R. China.
Guangfu JinDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Hongxia MaDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Zhibin HuDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Erbao ZhangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, P. R. China.
Fengwei TanDepartment of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, P. R. China.
Hongbing ShenDepartment of Epidemiology, School of Public Health, Southeast University, Nanjing, Jiangsu, 210009, P. R. China.
Nanjing Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNAcademy of Medical Sciences · GBSoutheast University · CNWuxi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpigenetic alterations have been shown to contribute immensely to human carcinogenesis. Dynamic and reversible N6-methyladenosine (m6A) RNA modification regulates gene expression and cell fate. However, the reasons for activation of KIAA1429 (also known as VIRMA, an RNA methyltransferase) and its underlying mechanism in lung adenocarcinoma (LUAD) remain largely unexplored. In this study, we aimed to clarify the oncogenic role of KIAA1429 in the tumorigenesis of LUAD.

methodsWhole-genome sequencing and transcriptome sequencing of LUAD data were used to analyze the gene amplification of RNA methyltransferase. The in vitro and in vivo functions of KIAA1429 were investigated. Transcriptome sequencing, methylated RNA immunoprecipitation sequencing (MeRIP-seq), m6A dot blot assays and RNA immunoprecipitation (RIP) were performed to confirm the modified gene mediated by KIAA1429. RNA stability assays were used to detect the half-life of the target gene.

resultsCopy number amplification drove higher expression of KIAA1429 in LUAD, which was correlated with poor overall survival. Manipulating the expression of KIAA1429 could regulate the proliferation and metastasis of LUAD. Mechanistically, the target genes of KIAA1429-mediated m6A modification were confirmed by transcriptome sequencing and MeRIP-seq assays. We also revealed that KIAA1429 could regulate BTG2 expression in an m6A-dependent manner. Knockdown of KIAA1429 significantly decreased the m6A levels of BTG2 mRNA, leading to enhanced YTH m6A RNA binding protein 2 (YTHDF2, the m6A "reader")-dependent BTG2 mRNA stability and promoted the expression of BTG2; thus, participating in the tumorigenesis of LUAD.

conclusionsOur data revealed the activation mechanism and important role of KIAA1429 in LUAD tumorigenesis, which may provide a novel view on the targeted molecular therapy of LUAD.

Indexed as

Adenocarcinoma of LungImmediate-Early ProteinsLung NeoplasmsRNA-Binding ProteinsTumor Suppressor ProteinsCarcinogenesisGene AmplificationHumansMethyltransferasesPrognosisRNABTG2 protein, humanImmediate-Early ProteinsMethyltransferasesRNARNA-Binding ProteinsTumor Suppressor ProteinsVIRMA protein, humanYTHDF2 protein, humanBTG2gene amplificationKIAA1429LUADmRNA stabilityN6-methyladenosineRNA methyltransferaseYTHDF2

Identifiers

PMID35730068
PMCPMC9257983
OpenAlexW4283315422

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.