Evidence map›Paper›PMID 33094561›Full record

ArticleJournal of cellular and molecular medicine2020

IGF2BP3 facilitates cell proliferation and tumorigenesis via modulation of JAK/STAT signalling pathway in human bladder cancer.

Wei Huang, Yuanyuan Li, Cheng Zhang, Huihai Zha, Xiaocheng Zhou, Bin Fu, Ju Guo, Gongxian Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

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  12. IGF2BP3 As a Prognostic Biomarker and Regulator of Metastasis in Merkel Cell Carcinoma.JID innovations : skin science from molecules to population health · 2025
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15 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

8 authors at 1 institution in 1 country.

Wei HuangDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0001-8311-8490
Yuanyuan LiDepartment of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Cheng ZhangDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Huihai ZhaDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Xiaocheng ZhouDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Bin FuDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Ju GuoDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Gongxian WangDepartment of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor-2 messenger RNA-binding protein 3 (IGF2BP3) has been reported to contribute to tumorigenesis in several human cancers. However, the biological functions of IGF2BP3 in bladder cancer are poorly understood. We investigated the relation between IGF2BP3 expression and prognosis of bladder cancer patients. Cell proliferation, cell cycle and cell apoptosis assays were performed to assess IGF2BP3 functions. The results showed that IGF2BP3 was overexpressed in bladder cancer tissues compared with that in normal bladder tissues, and its higher expression was closely correlated with poor prognosis in bladder cancer patients. Overexpression of IGF2BP3 markedly promoted cell proliferation and cell cycle progression and inhibited cell apoptosis, while knockdown of IGF2BP3 notably suppressed the proliferation, promoted cell apoptosis and induced cell cycle arrest at the G0/G1 phase. Mechanistically, we revealed that IGF2BP3 promotes the activation of the JAK/STAT pathway in bladder cancer cells. Moreover, the JAK/STAT inhibitor dramatically blocked the tumour-promoting activity of IGF2BP3. Tumour growth in vivo was also suppressed by knocking down of IGF2BP3. Hence, IGF2BP3 facilitated bladder cancer cell proliferation by activating the JAK/STAT signalling pathway. These findings suggest that IGF2BP3 exhibits an oncogenic effect in human bladder cancer progression.

Indexed as

Cell Transformation, NeoplasticSignal TransductionAdultAgedAnimalsApoptosisBiomarkersCell Cycle CheckpointsDatabases, GeneticDisease Models, AnimalFemaleHeterograftsHumansImmunohistochemistryJanus KinasesMaleBiomarkersIGF2BP3 protein, humanJanus KinasesRNA-Binding ProteinsSTAT Transcription Factorsbladder cancerIGF2BP3JAK/STATprognosisproliferation

Identifiers

PMID33094561
PMCPMC7753985
OpenAlexW3093726628

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.