Evidence map›Paper›PMID 30348215›Full record

ArticleClinical epigenetics2018

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma.

Yu Zheng, Baihui Li, Jian Wang, Yanjuan Xiong, Kaiyuan Wang, Ying Qi, Houfang Sun, Lei Wu, Lili Yang

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

9 authors at 1 institution in 1 country.

Yu ZhengDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Baihui LiDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Jian WangDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Yanjuan XiongDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Kaiyuan WangDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Ying QiDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Houfang SunDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Lei WuDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Lili YangDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. yanglili@tjmuch.com.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSUV39H2 (suppressor of variegation 3-9 homolog 2), which introduces H3K9me3 to induce transcriptional repression, has been reported to play critical roles in heterochromatin maintenance, DNA repair, and recently, carcinogenesis. Dysregulation of SUV39H2 expression has been observed in several types of cancers. However, neither the genomic landscape nor the clinical significance of SUV39H2 in lung adenocarcinoma has been probed comprehensively.

methodsIn this research, we conducted bioinformatics analysis to primarily sort out potential genes with dysregulated expressions. After we identified SUV39H2, RNA-seq was performed for a high-throughput evaluation of altered gene expression and dysregulated pathways, followed by a series of validations via RT-qPCR and bioinformatics analyses. Finally, to assess the potential oncogenic role of SUV39H2, we employed the invasion assay and clone formation assay in vitro and tumorigenesis assays in mouse models in vivo.

resultsThrough bioinformatics analyses, we found that SUV39H2 underwent a severe upregulation in the tumor tissue, which was also confirmed in the surgically removed tissues. Overexpression of SUV39H2 was mainly associated with its amplification and with shorter patient overall survival. Then, the RNA-seq demonstrated that TPM4, STOM, and OPTN might be affected by the loss of function of SUV39H2. Finally, in vitro and in vivo experiments with SUV39H2 knockdown all suggested a potential role of SUV39H2 in both carcinogenesis and metastasis.

conclusionsSUV39H2 expression was elevated in lung adenocarcinoma. TPM4, OPTN, and STOM were potentially regulated by SUV39H2. SUV39H2 might be a potential oncogene in lung adenocarcinoma, mediating tumorigenesis and metastasis.

Indexed as

Up-RegulationA549 CellsAdenocarcinoma of LungAnimalsCell Cycle ProteinsCell Line, TumorFemaleGene AmplificationGene Expression ProfilingGene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHumansLung NeoplasmsMaleMCF-7 CellsMembrane ProteinsCell Cycle ProteinsHistone-Lysine N-MethyltransferaseMembrane ProteinsMembrane Transport ProteinsOPTN protein, humanSTOM protein, humanSUV39H2 protein, humanTranscription Factor TFIIIA

Identifiers

PMID30348215
PMCPMC6198372
OpenAlexW2896420094

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.