Evidence map›Paper›PMID 32705243›Full record

ArticleInternational journal of oncology2020

SMYD3 overexpression indicates poor prognosis and promotes cell proliferation, migration and invasion in non‑small cell lung cancer.

Jing Li, Lifang Zhao, Yunjian Pan, Xiao Ma, Li Liu, Wuzhang Wang, Wenjie You

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2020. 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
1.5field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

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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

7 authors at 4 institutions in 1 country.

Jing Li *Department of Respiratory and Critical Care Medicine, Shandong Provincial Chest Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Lifang Zhao *Department of Respiratory and Critical Care Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China.
Yunjian PanDepartment of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Xiao MaDepartment of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Li LiuDepartment of Respiratory and Critical Care Medicine, Shandong Provincial Chest Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Wuzhang WangDepartment of Respiratory and Critical Care Medicine, Shandong Provincial Chest Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Wenjie YouDepartment of Respiratory and Critical Care Medicine, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250021, P.R. China.
Shandong University · CNFudan University Shanghai Cancer Center · CNShandong Chest Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SET and MYND domain‑containing protein 3 (SMYD3) is a lysine methyltransferase, and its aberrant expression has been implicated in several malignancies. However, its clinical and biological roles in non‑small cell lung cancer (NSCLC) remain unclear. In the present study, it was revealed that SMYD3 was significantly upregulated in NSCLC tissues, as compared with paired adjacent normal tissues. A high SMYD3 expression was associated with aggressive clinicopathological characteristics, as well as poor disease‑free survival and overall survival (OS) in NSCLC patients. Multivariate analysis revealed that SMYD3 overexpression was an independent predictor of poor OS in NSCLC patients. In addition, SMYD3 knockdown inhibited cell proliferation, triggered apoptosis, and blocked migration and invasion in NSCLC cells in vitro, whereas stable SMYD3 overexpression promoted NSCLC cell proliferation. Furthermore, the SMYD3‑silenced NSCLC cells became more sensitive, whereas the SMYD3‑overexpressed NSCLC cells became more resistant to the apoptosis induced by cisplatin. Mechanistic analysis revealed that SMYD3 knockdown led to the upregulation of Bim, Bak and Bax, and the downregulation of Bcl‑2, Bcl‑xl, MMP‑2 and MMP‑9 in NSCLC cells. In combination, the present findings indicated that SMYD3 has oncogenic potential in the context of NSCLC, providing evidence that may be exploited for both prognostic and therapeutic purposes in the future.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsApoptosisCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCisplatinDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesHistone-Lysine N-MethyltransferaseHumansKaplan-Meier EstimateLungAntineoplastic AgentsCisplatinHistone-Lysine N-MethyltransferaseSMYD3 protein, humancisplatin resistanceinvasionmigrationnon-small cell lung cancerprognostic markerproliferationSET and MYND domain-containing protein 3

Identifiers

PMID32705243
PMCPMC7384847
OpenAlexW3040076380

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.