Evidence map›Paper›PMID 36737782›Full record

ArticleJournal of translational medicine2023

Loss of miR-26b-5p promotes gastric cancer progression via miR-26b-5p-PDE4B/CDK8-STAT3 feedback loop.

Tingting Xu, Mengyan Xie, Xinming Jing, Huning Jiang, Xi Wu, Xinzhu Wang, Yongqian Shu

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  15. [Prognostic Value of PCMT1 Expression in Gastric Cancer and Its Regulatory Effect on Spindle Assembly Checkpoints].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023
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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 2 institutions in 1 country.

Tingting XuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mengyan XieDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xinming JingDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Huning JiangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xi WuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xinzhu WangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. shuyongqian2018@163.com.ORCID 0000-0003-0802-1677
Jiangsu Province Hospital · CNSuzhou Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic inflammation is a well-known risk factor for the development of gastric cancer (GC). Nevertheless, the molecular mechanisms underlying inflammation-related GC progression are incompletely defined.

methodsBioinformatic analysis was performed based on data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and the expression of miR-26b-5p in GC cells and tissues was validated by quantitative real-time PCR (qRT-PCR). Cell proliferation was examined through Cell Counting Kit-8 (CCK8), 5-Ethynyl-2'-deoxyuridine (EdU), colony formation, flow cytometry, and tumor xenografts. Correlation between miR-26b-5p and Cyclin dependent kinase 8 (CDK8) or Phosphodiesterase 4B (PDE4B) was analyzed by dual-luciferase reporter assays, qRT-PCR, and Western blot. The effect of miR-26b-5p on the Signal transducer and activator of transcription 3 (STAT3) pathway was investigated using Western blot, immunofluorescence (IF), and immunohistochemistry (IHC). The impact of STAT3 on miR-26b-5p was determined by dual-luciferase reporter assays and qRT-PCR.

resultsThe expression of miR-26b-5p was significantly downregulated in Helicobacter Pylori (H. pylori)-infected GC cells. The decreased expression of miR-26b-5p was also detected in GC cells and tissues compared to normal gastric epithelium cells (GES1) and normal adjacent gastric tissues. The low expression of miR-26b-5p promoted GC proliferation in vitro and in vivo and was related to the poor outcome of GC patients. In terms of mechanism, miR-26b-5p directly targeted PDE4B and CDK8, resulting in decreased phosphorylation and nuclear translocation of STAT3, which was associated with the regulation of GC proliferation by miR-26b-5p. Notably, miR-26b-5p was transcriptionally suppressed by STAT3, thus forming the miR-26b-5p-PDE4B/CDK8-STAT3 positive feedback loop.

conclusionThe newly identified miR-26b-5p-PDE4B/CDK8-STAT3 feedback loop plays an important role in inflammation-related GC progression and may serve as a promising therapeutic target for GC.

Indexed as

MicroRNAsStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationCyclic Nucleotide Phosphodiesterases, Type 4Cyclin-Dependent Kinase 8FeedbackGene Expression Regulation, NeoplasticHumansSTAT3 Transcription FactorCDK8 protein, humanCyclic Nucleotide Phosphodiesterases, Type 4Cyclin-Dependent Kinase 8MicroRNAsMIRN26 microRNA, humanPDE4B protein, humanSTAT3 protein, humanSTAT3 Transcription FactorGastric cancerInflammationmiR-26b-5pSTAT3

Identifiers

PMID36737782
PMCPMC9898947
OpenAlexW4319069256

What OpenQuestion holds

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LicenceCC BY
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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.