Evidence map›Paper›PMID 26129688›Full record

ArticleCancer medicine2015

Epigenetically altered miR-193b targets cyclin D1 in prostate cancer.

Kirsi M Kaukoniemi, Hanna E Rauhala, Mauro Scaravilli, Leena Latonen, Matti Annala, Robert L Vessella, Matti Nykter, Teuvo L J Tammela, Tapio Visakorpi

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Kirsi M KaukoniemiInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Hanna E RauhalaInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Mauro ScaravilliInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Leena LatonenInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Matti AnnalaInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Robert L VessellaDepartment of Urology, University of Washington, Seattle, Washington.
Matti NykterInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Teuvo L J TammelaDepartment of Urology, University of Tampere and Tampere University Hospital, Tampere, Finland.
Tapio VisakorpiInstitute of Biosciences and Medical Technology - BioMediTech, University of Tampere, Tampere, Finland.
Tampere University · FITampere University Hospital · FITampere University · FIUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Micro-RNAs (miRNA) are important regulators of gene expression and often differentially expressed in cancer and other diseases. We have previously shown that miR-193b is hypermethylated in prostate cancer (PC) and suppresses cell growth. It has been suggested that miR-193b targets cyclin D1 in several malignancies. Here, our aim was to determine if miR-193b targets cyclin D1 in prostate cancer. Our data show that miR-193b is commonly methylated in PC samples compared to benign prostate hyperplasia. We found reduced miR-193b expression (P < 0.05) in stage pT3 tumors compared to pT2 tumors in a cohort of prostatectomy specimens. In 22Rv1 PC cells with low endogenous miR-193b expression, the overexpression of miR-193b reduced CCND1 mRNA levels and cyclin D1 protein levels. In addition, the exogenous expression of miR-193b decreased the phosphorylation level of RB, a target of the cyclin D1-CDK4/6 pathway. Moreover, according to a reporter assay, miR-193b targeted the 3'UTR of CCND1 in PC cells and the CCND1 activity was rescued by expressing CCND1 lacking its 3'UTR. Immunohistochemical analysis of cyclin D1 showed that castration-resistant prostate cancers have significantly (P = 0.0237) higher expression of cyclin D1 compared to hormone-naïve cases. Furthermore, the PC cell lines 22Rv1 and VCaP, which express low levels of miR-193b and high levels of CCND1, showed significant growth retardation when treated with a CDK4/6 inhibitor. In contrast, the inhibitor had no effect on the growth of PC-3 and DU145 cells with high miR-193b and low CCND1 expression. Taken together, our data demonstrate that miR-193b targets cyclin D1 in prostate cancer.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticRNA Interference3' Untranslated RegionsCell Line, TumorCyclin D1DNA MethylationHumansMaleMicroRNAsNeoplasm GradingNeoplasm Recurrence, LocalNeoplasm StagingProstatic NeoplasmsRNA, Messenger3' Untranslated RegionsCyclin D1MicroRNAsMIRN193 microRNA, humanRNA, MessengerCyclin D1micro-RNAprostate cancer

Identifiers

PMID26129688
PMCPMC4567026
OpenAlexW1567311406

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.