Evidence map›Paper›PMID 32780563›Full record

ArticleCancer medicine2020

MiR-5683 suppresses glycolysis and proliferation through targeting pyruvate dehydrogenase kinase 4 in gastric cancer.

Yongchang Miao, Qing Li, Guangli Sun, Lu Wang, Diancai Zhang, Hao Xu, Zekuan Xu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Time- and dose-dependent regulation of circular RNAs in the response of triple-negative breast cancer cells to ionizing radiation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. MicroRNA-597 Suppresses Gastric Cancer Invasion and Progression viaInternational journal of molecular sciences · 2026
    Article
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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 3 institutions in 1 country.

Yongchang MiaoDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qing LiSchool of Medicine, Southeast University, Nanjing, China.
Guangli SunDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lu WangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Diancai ZhangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Hao XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zekuan XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-0882-3883
Jiangsu Province Hospital · CNSoutheast University · CNThe First People’s Hospital of Lianyungang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most deadly malignancies at global scale, and is particularly common in eastern Asia. MicroRNA-5683 (miR-5683) was confirmed to be downregulated in GC by analyzing data from the Cancer Genome Atlas. We packaged miR-5683-mimics and miR-5683-inhibitors into lentivirus vectors and transfected them into GC cells. MiR-5683 expression and possible target genes were detected by employing quantitative real-time polymerase chain reaction. In vitro, cell proliferation and apoptosis were analyzed using CCK-8, colony formation assay, and flow cytometric assay. We verified the direct interaction between miR-5683 and the possible downstream target gene pyruvate dehydrogenase kinase 4 (PDK4) through luciferase reporter assay. The role of miR-5683 in vivo was explored by injecting stably transfected GC cells subcutaneously into nude mice. Here we show that miR-5683 was downregulated in GC and the decreased level of miR-5683 enhances GC cell proliferation and impairs apoptosis. Tumor oncogene PDK4, which is associated with GC overall survival and disease-free survival, has been identified as the target gene of miR-5683. Besides, we demonstrate that the inhibition of miR-5683 promotes glycolysis by upregulating the PDK4 expression, thus leading to GC progression. Our study determines that miR-5683 represses GC glycolysis and progression through targeting PDK4. MiR-5683 overexpression may thus become a new treatment strategy for GC.

Indexed as

Cell ProliferationGlycolysisAnimalsApoptosisCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMice, NudeMicroRNAsMiddle AgedPyruvate Dehydrogenase Acetyl-Transferring KinaseSignal TransductionStomach NeoplasmsTumor BurdenMicroRNAsMIRN-569 microRNA, humanPDK4 protein, humanPyruvate Dehydrogenase Acetyl-Transferring Kinasegastric cancerglycolysismiR-5683proliferationpyruvate dehydrogenase kinase 4

Identifiers

PMID32780563
PMCPMC7541129
OpenAlexW3048840875

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.