Evidence map›Paper›PMID 42045037›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026

[Overexpression of miR-593-5p inhibits migration, invasion and proliferation and promotes apoptosis of gastric cancer cells by targeting PLK1].

Baolong Dong, Jiangshan Peng, Jinru Li, Yun Meng, Xiaojun Yang

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In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Baolong DongDepartment of General Surgery, Gansu University of Chinese Medicine, Lanzhou 730000, China.
Jiangshan PengDepartment of General Surgery, Gansu University of Chinese Medicine, Lanzhou 730000, China.
Jinru LiFirst Clinical Medicine College, Gansu University of Chinese Medicine, Lanzhou 730000, China.
Yun MengDepartment of General Surgery, Gansu University of Chinese Medicine, Lanzhou 730000, China.
Xiaojun YangDepartment of General Surgery, Gansu University of Chinese Medicine, Lanzhou 730000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo explore the role of miR-593-5p targeting Polo-like kinase 1 (PLK1) in regulating biological behaviors of human gastric cancer (GC) cells.

methodsFour GC cell lines (MGC-803, AGS, HGC-27, and MKN-45) and normal human gastric mucosal epithelial GES-1 cells were examined for miR-593-5p and PLK1 expressions using RT-PCR, and MGC-803 cells with the lowest miR-593-5p expression and MKN-45 with highest miR-593-5p expression were selected for subsequent experiments. TargetScan7.2 was used to predict the binding between miR-593-5p and PLK1. MGC-803 cells were transfected with miR-593-5p mimic or mimic NC via liposome, and MKN-45 cells were transfected with miR-593-5p inhibitor or inhibitor NC. The changes in cellular PLK1 protein expression levels were detected using Western blotting, and the changes in biological behaviors of the cells were evaluated using scratch assay, Transwell assay, CCK-8 assay, and flow cytometry.

resultsCompared with GES-1 cells, the GC cell lines showed significantly downregulated miR-593-5p and upregulated PLK1 expressions. TargetScan7.2 identified binding sites between miR-593-5p and PLK1 3'UTR. In MGC-803 cells, miR-593-5p overexpression caused significant reduction of PLK1 protein expression, inhibited cell migration, invasion, and proliferation, and promoted cell apoptosis. Conversely, miR-593-5p inhibition in MKN-45 cells upregulated PLK1 expression, enhanced cell migration, invasion, and proliferation, reduced cell apoptosis.

conclusionsmiR-593-5p overexpression inhibits GC cell migration, invasion, and proliferation, and promotes apoptosis, likely by directly downregulating PLK1, suggesting the role of miR-593-5p as a tumor suppressor in GC and its potential therapeutic relevance.

Indexed as

ApoptosisCell Cycle ProteinsMicroRNAsProtein Serine-Threonine KinasesProto-Oncogene ProteinsStomach NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPolo-Like Kinase 1Cell Cycle ProteinsMicroRNAsMIRN593 microRNA, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsBiological functiongastric cancermiR-593-5pPLK1

Identifiers

PMID42045037
PMCPMC13120992

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