Evidence map›Paper›PMID 23279696›Full record

ArticleCancer science2013

ALKBH2, a novel AlkB homologue, contributes to human bladder cancer progression by regulating MUC1 expression.

Tomomi Fujii, Keiji Shimada, Satoshi Anai, Kiyohide Fujimoto, Noboru Konishi

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Predictive Analysis and Validation of Critical Missense SNPs of theInternational journal of molecular sciences · 2025
    Review
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  6. Article
  7. Research progress of MUC1 in genitourinary cancers.Cellular & molecular biology letters · 2024
    Review
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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

5 authors at 2 institutions in 1 country.

Tomomi FujiiDepartment of Pathology, Nara Medical University School of Medicine, Nara, Japan.
Keiji Shimada
Satoshi Anai
Kiyohide Fujimoto
Noboru Konishi
Nara Medical University Hospital · JPNara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ALKBH family of proteins are highly expressed in various types of human cancer where they are involved in tumor growth and progression. However, multiple isoforms of ALKBH exist and the effect of individual isoforms on the development of urinary bladder cancer is unknown, particularly the molecular mechanisms involved in the progression from a noninvasive to invasive phenotype. We examined the role and function of ALKBH2 in human bladder cancer development in vitro and provide the first report that suppression of ALKBH2 in a human urothelial carcinoma cell line, KU7, reduces the expression of the transmembrane mucin protein, MUC1, and induces G1 cell cycle arrest. Moreover, reduction of ALKBH2 suppressed epithelial to mesenchymal transition (EMT) via increasing E-cadherin and decreasing vimentin expression. Transfection of MUC1 siRNA inhibited cell proliferation and EMT to the same extent as ALKBH2 gene silencing in vitro. ALKBH2 knockdown significantly suppressed MUC1 expression and tumor volume of bladder cancers in vivo as assessed in an orthotopic mouse model using ALKBH2 shRNA transfected KU7 cells. Immunohistochemical examination showed high expression levels of ALKBH2 in human urothelial carcinoma samples, especially in high-grade, superficially and deeply invasive carcinomas (pT(1) and >pT(2)), and in carcinoma in situ but not in normal urothelium. This study demonstrates that ALKBH2 is an upstream molecule of the oncoprotein, MUC1, and regulates cell cycle and EMT, resulting in progression of urothelial carcinomas.

Indexed as

Gene Expression Regulation, NeoplasticAlkB Homolog 2, Alpha-Ketoglutarate-Dependent DioxygenaseAnimalsCadherinsCell Cycle CheckpointsCell Line, TumorCell ProliferationDioxygenasesDisease ProgressionDNA Repair EnzymesEpithelial-Mesenchymal TransitionGene SilencingHumansMiceMucin-1Neoplasm TransplantationALKBH2 protein, humanAlkB Homolog 2, Alpha-Ketoglutarate-Dependent DioxygenaseCadherinsDioxygenasesDNA Repair EnzymesMucin-1Vimentin

Identifiers

PMID23279696
PMCPMC7657176
OpenAlexW2012514086

What OpenQuestion holds

Textmetadata
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.