Evidence map›Paper›PMID 30886505›Full record

ArticleWorld journal of gastroenterology2019

MicroRNA-596 acts as a tumor suppressor in gastric cancer and is upregulated by promotor demethylation.

Zhen Zhang, Dong-Qiu Dai

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. MicroRNA-596 is epigenetically inactivated and suppresses prostatic cancer cell growth and migration via regulating Wnt/β-catenin signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  6. Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Zhen ZhangDepartment of Gastroenterological Surgery, the Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China.
Dong-Qiu DaiDepartment of Gastroenterological Surgery, the Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China. daidq63@163.com.
Fourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn the present study, we investigated a suppressive role of microRNA-596 (miR-596) in gastric cancer (GC). Moreover, the downregulation of miR-596 in GC cell lines was associated with an increase of miR-596 promoter methylation. We also established that miR-596 controls the expression of peroxiredoxin 1 (PRDX1), which has never been reported before, suggesting that this interaction could play an important role in GC progression.

aimTo study the potential role and possible regulatory mechanism of miR-596 in GC.

methodsThe expression levels of miR-596 and PRDX1 in gastric cancer tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR). Western blot and luciferase reporter assay were used to detect the effect of miR-596 on PRDX1 expression. Then, the proliferation, metastasis, and invasion of GC cell lines transfected with miR-596 mimics were analyzed, respectively, by Cell Counting Kit-8 proliferation assay, wound healing assay, and transwell invasion assay. Meanwhile, the methylation status of the promoter CpG islands of miR-596 in GC cell lines was detected by methylation-specific PCR (MSP).

resultsExpression of miR-596 was decreased and PRDX1 was upregulated in GC tissues and cell lines. Overexpression of miR-596 decreased the expression of PRDX1 and luciferase reporter assays detected the direct binding of miR-596 to the 3'-untranslated region (UTR) of PRDX1 transcripts. Furthermore, we found that overexpression of miR-596 remarkably suppressed cell proliferation, migration, and invasion in GC cells. We further analyzed miR-596 promoter methylation by MSP and qRT-PCR, and found the downregulation of miR-596 was associated with promoter methylation status in GC cell lines. Moreover, DNA demethylation and reactivation of miR-596 after treatment with 5-Aza-2'-deoxycytidine inhibited the proliferative ability of GC cells.

conclusionMiR-596 has a tumor suppressive role in GC and is downregulated partly due to promoter hypermethylation. Furthermore, PRDX1 is one of the putative target genes of miR-596.

Indexed as

Genes, Tumor SuppressorCell Line, TumorCell ProliferationCpG IslandsDecitabineDisease ProgressionDNA DemethylationDNA MethylationDown-RegulationGene Expression Regulation, NeoplasticHumansMicroRNAsPeroxiredoxinsPromoter Regions, GeneticStomachStomach NeoplasmsDecitabineMicroRNAsMIRN596 microRNA, humanPeroxiredoxinsPRDX1 protein, humanGastric cancerMethylationMicroRNA-596Peroxiredoxin 1

Identifiers

PMID30886505
PMCPMC6421237
OpenAlexW2921713103

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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.