Evidence map›Paper›PMID 27078844›Full record

ArticleOncotarget2016

MicroRNA-26b inhibits tumor metastasis by targeting the KPNA2/c-jun pathway in human gastric cancer.

Ming-Ming Tsai, Hsiang-Wei Huang, Chia-Siu Wang, Kam-Fai Lee, Chung-Ying Tsai, Pei-Hsuan Lu, Hsiang-Cheng Chi, Yang-Hsiang Lin, Liang-Mou Kuo, Kwang-Huei Lin

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.1field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Ming-Ming TsaiDepartment of Nursing, Division of Basic Medical Sciences and Research Center for Industry of Human Ecology, Chang-Gung University of Science and Technology, Taoyuan, 333, Taiwan.
Hsiang-Wei HuangDepartment of Biochemistry, College of Medicine, Chang-Gung University, Taoyuan, 333, Taiwan.
Chia-Siu WangDepartment of General Surgery, Chang Gung Memorial Hospital at Chia-yi, Chia-yi, 613, Taiwan.
Kam-Fai LeeDepartment of Pathology, Chang Gung Memorial Hospital, Chia-yi, 613, Taiwan.
Chung-Ying TsaiDepartment of Biochemistry, College of Medicine, Chang-Gung University, Taoyuan, 333, Taiwan.
Pei-Hsuan LuDepartment of Dermatology, Chang Gung Memorial Hospital, Chang Gung University, Taipei, 10508, Taiwan.
Hsiang-Cheng ChiDepartment of Biochemistry, College of Medicine, Chang-Gung University, Taoyuan, 333, Taiwan.
Yang-Hsiang LinDepartment of Biochemistry, College of Medicine, Chang-Gung University, Taoyuan, 333, Taiwan.
Liang-Mou KuoDepartment of General Surgery, Chang Gung Memorial Hospital at Chia-yi, Chia-yi, 613, Taiwan.
Kwang-Huei LinDepartment of Biochemistry, College of Medicine, Chang-Gung University, Taoyuan, 333, Taiwan.
Chang Gung University · TWChiayi Chang Gung Memorial Hospital · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNA) play an important role in carcinogenesis. Previously, we identified miR-26b as a significantly downregulated miRNA in gastric cancer (GC) tissues (n = 106) based on differential quantitative RT-PCR (RT-qPCR) miRNA expression profiles. In the current study, we aimed to clarify the potential role of miR-26b and related target genes in GC progression. Downregulation of miR-26b was associated with advanced tumor-node-metastasis stage (TNM stage) and poor 5-year survival rate. Forced expression of miR-26b led to inhibition of GC cell migration and invasion in vitro and lung metastasis formation in vivo. Conversely, depletion of miR-26b had stimulatory effects. Additionally, miR-26b affected GC cell behavior through negative regulation of the metastasis promoter, karyopherin alpha 2 (KPNA2). Ectopic expression of miR-26b induced a reduction in KPNA2 protein levels, confirmed by luciferase assay data showing that miR-26b directly binds to the 3' untranslated regions (UTR) of KPNA2 mRNA. Furthermore, miR-26b and KPNA2 mRNA/protein expression patterns were inversely correlated in GC tissues. Cag A of Helicobacter pylori (Hp) enhanced miR-26b levels through regulation of the KPNA2/c-jun pathway. Taken together, our data indicate that miR-26b plays an anti-metastatic role and is downregulated in GC tissues via the KPNA2/c-jun pathway. Based on the study findings, we propose that miR-26b overexpression or KPNA2/c-jun suppression may have therapeutic potential in inhibiting GC metastasis.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdultAgedAged, 80 and overalpha KaryopherinsAntigens, BacterialBacterial ProteinsCell Line, TumorCell MovementDisease ProgressionFemaleHelicobacter pyloriHumansMaleMicroRNAs3' Untranslated Regionsalpha KaryopherinsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriKPNA2 protein, humanMicroRNAsMIRN26 microRNA, humanProto-Oncogene Proteins c-junc-jungastric cancerKPNA2miR-26bprognosis

Identifiers

PMID27078844
PMCPMC5129949
OpenAlexW2328788814

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.