Evidence map›Paper›PMID 32284070›Full record

ArticleWorld journal of surgical oncology2020

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway.

Haiyan Zhang, Lingyun Li, Cuicui Yuan, Congcong Wang, Tiantian Gao, Zhiwei Zheng

Open access · goldAbstract read
In one paragraph

Article in World journal of surgical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
  8. HDAC7: a promising target in cancer.Frontiers in oncology · 2024
    Review
  9. Histone Modification of Colorectal Cancer by Natural Products.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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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

6 authors at 3 institutions in 1 country.

Haiyan ZhangDepartment of Gastroenterology, People's Hospital of Rizhao, Rizhao, 276800, China.
Lingyun LiDepartment of Internal Medicine, Laishan Branch Hospital of Yantai Yuhuangding Hospital, Yantai, 264003, China.
Cuicui YuanDepartment of Cardiovascular Medicine, The People's Hospital of zhangqiu area, Jinan, 250200, China.
Congcong WangDepartment of Operation Room, The People's Hospital of zhangqiu area, Jinan, 250200, China.
Tiantian GaoDepartment of Nephrology, The People's Hospital of zhangqiu area, Jinan, 250200, China.
Zhiwei ZhengDepartment of General Surgery, People's Hospital of Rizhao, 126, Tai'an Road, Rizhao, 276800, China. manmmtr@mail.com.
Zhangqiu City People's Hospital · CNPeople’s Hospital of Rizhao · CNYuhuangding Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMounting evidences have displayed that the dysregulation of miRNAs plays important roles in the pathogenesis of gastric cancer (GC). The purpose of this study was to explore the biological functions and potential mechanism of miR-489 in GC progression.

methodsQuantitative real-time PCR (qRT-PCR) and western blot were performed to examine the mRNA expression and protein levels of miR-489 and HDAC7. The relationship between miR-489 and HDAC7 was analyzed by Spearman rank correlation. 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays were conducted for determining the effect of miR-489 and HDAC7 on GC cell viability, migration, and invasion. TargetScan and luciferase reporter assay were used to confirm the target gene of miR-489 in GC cells.

resultsThe findings showed that miR-489 was dramatically decreased in GC tissues and GC cell lines (SGC-7901 and MKN45). Moreover, it was closely correlated with overall survival (OS) and progression-free survival (PFS) of GC patients. Downregulation of miR-489 significantly promoted GC cell proliferation, invasion, and migration. Additionally, HDAC7 was confirmed as the direct target of miR-489. Knockdown of HDAC7 exerted inhibited effect on GC progression and it markedly overturned miR-489 inhibitor-medicated effect on GC cells. More interestingly, via targeting HDAC7, miR-489 blocked the activation of PI3K/AKT pathway in GC cells.

conclusionsCorrectively, miR-489 played as a tumor suppressor in GC cell growth by targeting HDAC7, and miR-489 might function as a novel biomarker for diagnosis or therapeutic targets of human GC.

Indexed as

AdultAgedCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHistone DeacetylasesHumansMaleMicroRNAsMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionStomach NeoplasmsHDAC7 protein, humanHistone DeacetylasesMicroRNAsMIRN489 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktGastric cancerHDAC7miR-489PI3K/AKT pathway

Identifiers

PMID32284070
PMCPMC7155329
OpenAlexW3015979847

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.