Evidence map›Paper›PMID 26801246›Full record

ArticleMolecular cancer2016

miR-508-3p concordantly silences NFKB1 and RELA to inactivate canonical NF-κB signaling in gastric carcinogenesis.

Tingting Huang, Wei Kang, Bin Zhang, Feng Wu, Yujuan Dong, Joanna H M Tong, Weiqin Yang, Yuhang Zhou, Li Zhang, Alfred S L Cheng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  18. Exploration of the Important Role of Microfibril-Associated Protein 4 Gene in Oral Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  19. Article
  20. ChrXq27.3 miRNA cluster functions in cancer development.Journal of experimental & clinical cancer research : CR · 2021
    Review
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

12 authors at 4 institutions in 1 country.

Tingting HuangDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. huangtingting0531@gmail.com.
Wei KangDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. weikang@cuhk.edu.hk.
Bin ZhangDepartment of Gastroenterology, The Affiliated Drum Tower Hospital of Nanjing University, Medical School, Nanjing, PR China. billzhangnju@foxmail.com.
Feng WuDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. wufeng@link.cuhk.edu.hk.
Yujuan DongInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. celia.yj.dong@gmail.com.
Joanna H M TongDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. jtong@cuhk.edu.hk.
Weiqin YangShenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, PR China. weiqinyang1021@cuhk.edu.hk.
Yuhang ZhouDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. zyhjoe@gmail.com.
Li ZhangDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. yblhzl@hotmail.com.
Alfred S L ChengShenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, PR China. alfredcheng@cuhk.edu.hk.
Jun YuInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. junyu@cuhk.edu.hk.
Ka Fai ToDepartment of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. kfto@cuhk.edu.hk.
Chinese University of Hong Kong · CNChinese University of Hong Kong, Shenzhen · CNPrince of Wales Hospital · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNF-κB signaling pathway plays an important role in gastric carcinogenesis. The basic expression and functional role of NFKB1 and RELA (components of canonical NF-κB pathway) in gastric cancer (GC) have not been well elucidated. In this study, the role of NFKB1 and RELA in gastric tumorigenesis will be investigated and their regulation by microRNAs (miRNAs) will be deeply explored.

methodsThe mRNA and protein expression of NFKB1 and RELA were investigated by qRT-PCR and Western blot in GC cell lines and primary tumors. The functional roles of NFKB1 and RELA in GC were demonstrated by MTT proliferation assay, monolayer colony formation, cell invasion and migration, cell cycle analysis and in vivo study through siRNA mediated knockdown. Identification of NFKB1 as a direct target of tumor suppressor miRNA miR-508-3p was achieved by expression regulation assays together with dual luciferase activity experiments.

resultsNFKB1 and RELA were up-regulated in GC cell lines and primary tumors compared with normal gastric epithelium cells and their upregulation correlation with poor survival in GC. siRNA mediated knockdown of NFKB1 or RELA exhibited anti-oncogenic effect both in vitro and in vivo. NFKB1 was further revealed to be a direct target of miR-508-3p in gastric tumorigenesis and their expression showed negative correlation in primary GC samples. miR-508-3p was down-regulated in GC cells compared with normal gastric epithelium samples and its ectopic expression in GC cell lines also exerts tumor suppressor function. NFKB1 re-expression was found to partly abolish the tumor-suppressive effect of miR-508-3p in GC.

conclusionAll these findings supports that canonical NF-κB signaling pathway is activated in GC at least by the inactivation of miR-508-3p and this might have therapeutic potential in GC treatment.

Indexed as

Gene SilencingSignal TransductionBase SequenceCarcinogenesisCell Line, TumorDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMicroRNAsMiddle AgedMolecular Sequence DataMultivariate AnalysisNF-kappa B p50 SubunitMicroRNAsMIRN508 microRNA, humanNF-kappa B p50 SubunitNFKB1 protein, humanTranscription Factor RelA

Identifiers

PMID26801246
PMCPMC4724081
OpenAlexW2257985365

What OpenQuestion holds

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LicenceCC BY
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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.