Evidence map›Paper›PMID 34615858›Full record

ArticleCell death & disease2021

Elevated expression of nuclear receptor-binding SET domain 3 promotes pancreatic cancer cell growth.

Yihui Sun, Jiaming Xie, Shang Cai, Qian Wang, Zhenyu Feng, Yecheng Li, Jing-Jing Lu, Wei Chen, Zhenyu Ye

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. 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
1.2field-weighted citation impact, top 21% 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, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022
    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 2 institutions in 1 country.

Yihui Sun *Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jiaming Xie *Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Shang Cai *Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Qian Wang *Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Zhenyu FengDepartment of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Yecheng LiDepartment of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jing-Jing LuDepartment of Radiotherapy and Oncology, Affiliated Kunshan Hospital of Jiangsu University, Kunshan, China. marvel_j@163.com.ORCID 0000-0001-9938-2560
Wei ChenDepartment of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China. trybest1971@163.com.
Zhenyu YeDepartment of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China. yezhenyu1@163.com.ORCID 0000-0001-7174-0733
Soochow University · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nuclear receptor-binding SET domain 3 (NSD3) catalyzes methylation of histone H3 at lysine 36 (H3K36), and promotes malignant transformation and progression of human cancer. Its expression, potential functions and underlying mechanisms in pancreatic cancer are studied. Bioinformatics studies and results from local human tissues show that NSD3 is upregulated in human pancreatic cancer tissues, which is correlated with poor overall survival. In primary and established pancreatic cancer cells, NSD3 silencing (by shRNAs) or CRISPR/Cas9-induced NSD3 knockout potently inhibited cell proliferation, migration and invasion, while provoking cell cycle arrest and apoptosis. Conversely, ectopic expression of NSD3-T1232A mutation significantly accelerated proliferation, migration, and invasion of pancreatic cancer cells. H3K36 dimethylation, expression of NSD3-dependent genes (Prkaa2, Myc, Irgm1, Adam12, and Notch3), and mTOR activation (S6K1 phosphorylation) were largely inhibited by NSD3 silencing or knockout. In vivo, intratumoral injection of adeno-associated virus (AAV)-packed NSD3 shRNA potently inhibited pancreatic cancer xenograft growth in nude mice. These results suggest that elevated NSD3 could be an important driver for the malignant progression of pancreatic cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalCohort StudiesCRISPR-Cas SystemsHistone-Lysine N-MethyltransferaseHistonesHumansMethylationMiceMice, NudeMutationHistone-Lysine N-MethyltransferaseHistonesNSD3 protein, humanNuclear ProteinsRNA, MessengerRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID34615858
PMCPMC8494902
OpenAlexW3203540272

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.