Evidence map›Paper›PMID 25349215›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2015

Does Wnt/β-catenin pathway contribute to the stability of DNMT1 expression in urological cancer cell lines?

Nuray Varol, Ece Konac, Cenk Y Bilen

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Contrast effects of autophagy in the treatment of bladder cancer.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
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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

3 authors at 2 institutions in 1 country.

Nuray VarolDepartment of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, 06510 Ankara, Turkey.
Ece KonacDepartment of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, 06510 Ankara, Turkey ecemercanoglu@yahoo.com.
Cenk Y BilenDepartment of Urology, Faculty of Medicine, Hacettepe University, Sıhhiye, 06100 Ankara, Turkey.
Gazi University · TRHacettepe University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation is considered as one of the most important epigenetic mechanisms and it is catalyzed by DNA methyltransferases (DNMTs). DNMT1 abundance has been frequently seen in urogenital system tumors but the reasons for this abundance are not well understood. We aimed to look into the effects of Wnt/β-catenin signaling pathway on overexpression of DNMT1 and aberrant expression of UHRF1 and HAUSP which are responsible for stability of DNMT1 at transcriptional and protein levels in urogenital cancers. In this context, firstly, Wnt/β-catenin signaling pathway was activated by using SB216763 which is a glycogen synthase kinase-3 (GSK3) β inhibitor. Cell proliferation levels in bladder cancer cells, renal cell carcinoma, and prostate cancer cells treated with GSK3β inhibitor (SB216763) were detected by WST-1 reagent. WIF-1 gene methylation profile was determined by methylation-specific PCR (MSP); expression levels of target genes β-catenin and WIF-1 by real-time PCR; and protein levels of β-catenin, DNMT1, pGSK3β(Ser9), HAUSP, and UHRF1 by Western Blot. Our results indicated that treatment with SB216763 caused an increased cell proliferation at low dose. mRNA levels of β-catenin increased after treatment with SB216273 and protein levels of pGSK3β(Ser9), β-catenin, and DNMT1 increased in comparison to control. HAUSP and UHRF1 were either up-regulated or down-regulated at the same doses depending on the type of cancer. Also, we showed that protein levels of DNMT1, β-catenin, HAUSP, and UHRF1 decreased after re-expression of WIF-1 following treatment with DAC. In Caki-2 cells, β-catenin pathway might have accounted for the stability of DNMT1 expression, whereas such relation is not valid for T24 and PC3 cells. Our findings may offer a new approach for determination of molecular effects of Wnt/β-catenin signal pathway on DNMT1. This may allow us to identify new molecular targets for the treatment of urogenital cancers.

Indexed as

Adaptor Proteins, Signal Transducingbeta CateninCCAAT-Enhancer-Binding ProteinsCell Line, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationHumansIndolesMaleimidesPromoter Regions, GeneticReal-Time Polymerase Chain ReactionRepressor ProteinsRNA, MessengerUbiquitin-Protein LigasesAdaptor Proteins, Signal Transducingbeta CateninCCAAT-Enhancer-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanIndolesMaleimidesRepressor ProteinsRNA, MessengerSB 216763Ubiquitin-Protein LigasesUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseUHRF1 protein, humanUSP7 protein, humanWIF1 protein, humanWnt Proteinsdeubiquitinase HAUSP (USP7)DNA methyltransferase 1 stabilityE3 ubiquitin ligase UHRF1urological cancer cell linesWnt inhibitory factor-1Wnt/β-catenin pathway

Identifiers

PMID25349215
PMCPMC4935274
OpenAlexW1992999107

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.