Evidence map›Paper›PMID 28399871›Full record

ArticleMolecular cancer2017

IGF2BP3 functions as a potential oncogene and is a crucial target of miR-34a in gastric carcinogenesis.

Yuhang Zhou, Tingting Huang, Ho Lam Siu, Chi Chun Wong, Yujuan Dong, Feng Wu, Bin Zhang, William K K Wu, Alfred S L Cheng, Jun Yu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
4.2field-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

88 citing papers in PubMed, 146 citations in OpenAlex.

  1. mApplied biochemistry and biotechnology · 2026
    Article
  2. Adaptation of OXPHOS biogenesis to cellular requirements.Protein science : a publication of the Protein Society · 2026
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  10. hsa_circ_0007376 Promotes Gastric Cancer Proliferation and Malignant Metastasis by Enhancing the Stability of IGF2BP3.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025
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  17. IGF2BPs as novel mGenes & diseases · 2024
    Review
  18. Article
  19. NJournal of translational internal medicine · 2024
    Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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.

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, People's Republic of China.
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, People's Republic of China.
Ho Lam SiuDepartment 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, People's Republic of China.
Chi Chun WongPartner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
Yujuan DongPartner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
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, People's Republic of China.
Bin ZhangDepartment of Gastroenterology, The Affiliated Drum Tower Hospital of Nanjing University, Medical School, Nanjing, People's Republic of China.
William K K WuPartner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
Alfred S L ChengShenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, People's Republic of China.
Jun YuPartner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
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, People's Republic of China. kfto@cuhk.edu.hk.
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, People's Republic of China. weikang@cuhk.edu.hk.
Chinese University of Hong Kong · CNChinese University of Hong Kong, Shenzhen · CNNanjing Drum Tower Hospital · CNPrince of Wales Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer (GC) is one of the frequent causes of cancer-related death in eastern Asian population. IGF2BP2 lists in the top rank up-regulated genes in GC, but its functional role is unclear.

methodThe expression of IGF2BP3 in GC cell lines and primary samples was examined by qRT-PCR and Western blot. The biological role of IGF2BP3 was revealed by a series of functional in vitro studies. Its regulation by microRNAs (miRNAs) was predicted by TargetScan and confirmed by luciferase assays and rescue experiments.

resultsIGF2BP3 ranked the No.1 of the up-regulated genes by expression microarray analysis in GC cell lines. The expression level of IGF2BP3 was observed in GC tissues comparing with non-tumorous gastric epitheliums. The up-regulated IGF2BP3 expression was associated with poor disease specific survival. IGF2BP3 knockdown significantly inhibited cell proliferation and invasion. Apart from copy number gain, IGF2BP3 has been confirmed to be negatively regulated by tumor-suppressive miRNA, namely miR-34a. The expression of miR-34a showed negative correlation with IGF2BP3 mRNA expression in primary GC samples and more importantly, re-overexpression of IGF2BP3 rescued the inhibitory effect of miR-34a.

conclusionWe compressively revealed the oncogenic role of IGF2BP3 in gastric tumorigenesis and confirmed its activation is partly due to the silence of miR-34a. Our findings identified useful prognostic biomarker and provided clinical translational potential.

Indexed as

Gene Expression Regulation, NeoplasticOncogenesAnimalsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalGene SilencingHeterograftsHumansKaplan-Meier EstimateMiceMicroRNAsPrognosisRNA-Binding ProteinsRNA InterferenceStomach NeoplasmsIGF2BP3 protein, humanMicroRNAsMIRN34 microRNA, humanRNA-Binding ProteinsGastric cancerIGF2BP3miR-34a

Identifiers

PMID28399871
PMCPMC5387209
OpenAlexW2607257578

What OpenQuestion holds

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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.