Evidence map›Paper›PMID 28474805›Full record

ArticleCancer science2017

CLDN8, an androgen-regulated gene, promotes prostate cancer cell proliferation and migration.

Daisaku Ashikari, Ken-Ichi Takayama, Daisuke Obinata, Satoru Takahashi, Satoshi Inoue

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

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  9. Histone methyltransferase KMT2C plays an oncogenic role in prostate cancer.Journal of cancer research and clinical oncology · 2022
    Article
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  20. MiR-361-5p inhibits cell proliferation and induces cell apoptosis in retinoblastoma by negatively regulating CLDN8.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019
    Article
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.

Daisaku AshikariDepartment of Anti-Aging Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Ken-Ichi TakayamaDepartment of Anti-Aging Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Daisuke ObinataDepartment of Urology, Nihon University School of Medicine, Tokyo, Japan.
Satoru TakahashiDepartment of Urology, Nihon University School of Medicine, Tokyo, Japan.
Satoshi InoueDepartment of Anti-Aging Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-1247-3844
Nihon University · JPTokyo Metropolitan Institute of Gerontology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proliferation of prostate cancer cells is controlled by the androgen receptor (AR) signaling pathway. However, the function of AR target genes has not been fully elucidated. In previous studies, we have identified global AR binding sites and AR target genes in prostate cancer cells. Here, we focused on Claudin 8 (CLDN8), a protein constituting tight junctions in cell membranes. We found one AR binding site in the promoter region and two functional androgen-responsive elements in the sequence. Reporter assay revealed that transcriptional activation of the CLDN8 promoter by androgen is dependent on these androgen-responsive elements. Furthermore, CLDN8 mRNA is induced by androgen time-dependently and the induction is blocked by AR inhibitor, suggesting that AR is involved in the transcriptional activation. In addition, our functional analyses by overexpression and knockdown of CLDN8 mRNA indicate that CLDN8 promotes prostate cancer cell proliferation and migration. Claudin 8 was overexpressed in prostate cancer clinical samples compared to benign tissues. Furthermore, we found that CLDN8 regulates intracellular signal transduction and stabilizes the cytoskeleton. Taken together, these results indicate that CLDN8 functions as an AR downstream signal to facilitate the progression of prostate cancer. Claudin 8 may be a novel molecular target for prostate cancer therapy.

Indexed as

Cell MovementCell ProliferationBlotting, WesternChromatin ImmunoprecipitationClaudinsElectrophoretic Mobility Shift AssayGene Expression Regulation, NeoplasticHumansImmunohistochemistryMalePolymerase Chain ReactionProstatic NeoplasmsReceptors, AndrogenResponse ElementsTranscriptional Activationclaudin 8ClaudinsReceptors, AndrogenAndrogen receptorcell migrationcell proliferationCLDN8prostate cancer

Identifiers

PMID28474805
PMCPMC5497721
OpenAlexW2610636284

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.