Evidence map›Paper›PMID 28901481›Full record

ArticleOncology reports2017

Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis.

Zhiwei Liu, Lianhua Piao, Ming Zhuang, Xubin Qiu, Xiaoshuang Xu, Dawei Zhang, Mengmeng Liu, Ding Ren

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Biomedicines · 2024
    Article
  2. Review
  3. Review
  4. Review
  5. The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. 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

8 authors at 2 institutions in 1 country.

Zhiwei LiuDepartment of Orthopaedics, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213000, P.R. China.
Lianhua PiaoInstitute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, Changzhou, Jiangsu 213001, P.R. China.
Ming ZhuangDepartment of Orthopaedics, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213000, P.R. China.
Xubin QiuDepartment of Orthopaedics, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213000, P.R. China.
Xiaoshuang XuInstitute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, Changzhou, Jiangsu 213001, P.R. China.
Dawei ZhangInstitute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, Changzhou, Jiangsu 213001, P.R. China.
Mengmeng LiuInstitute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, Changzhou, Jiangsu 213001, P.R. China.
Ding RenOut-Patient Department, PLA No. 85th Hospital, Shanghai 200006, P.R. China.
Jiangsu University of Technology · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NSD3 is a histone lysine methyltransferase that methylates histone H3 at lysine 36. NSD3 is located at chromosome 8p11.23, the locus that exhibits strong cancer relevance. Thus, NSD3 is likely involved in multiple human cancers. Nevertheless, its roles in human carcinogenesis remain unknown. In the present study, we demonstrated that silencing of NSD3 in osteosarcoma, the most common primary bone cancer in children and adolescents, results in a marked decrease in the number of viable cancer cells, accompanied by increases in the cell population at the G2/M phase and the number of apoptotic cells. In addition, 549 NSD3‑regulated genes were identified and a set of selected candidate genes were validated. Bioinformatic analysis revealed that NSD3 negatively regulates a number of genes that are involved in the process of negative regulation of signal transduction as well as negative regulation of signaling and cell communication. Our results indicate the oncogenic roles of NSD3 in the development and progression of human osteosarcoma, and implicate NSD3 as a potential molecular target for selective therapy for human osteosarcoma.

Indexed as

Gene Regulatory NetworksAdolescentApoptosisBone NeoplasmsCell CycleCell Line, TumorCell SurvivalChildGene Expression Regulation, NeoplasticGene SilencingHistone-Lysine N-MethyltransferaseHumansNuclear ProteinsOsteosarcomaRNA, Small InterferingSequence Analysis, RNAHistone-Lysine N-MethyltransferaseNSD3 protein, humanNuclear ProteinsRNA, Small Interfering

Identifiers

PMID28901481
PMCPMC5780032
OpenAlexW2751763266

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.