Evidence map›Paper›PMID 19920820›Full record

ArticleBritish journal of cancer2009

Glycogen synthase kinase-3: a new therapeutic target in renal cell carcinoma.

V Bilim, A Ougolkov, K Yuuki, S Naito, H Kawazoe, A Muto, M Oya, D Billadeau, T Motoyama, Y Tomita

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.0field-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

62 citing papers in PubMed, 107 citations in OpenAlex.

  1. Review
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  6. The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024
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  14. Recent Approaches to Targeting Canonical NFJournal of the American Society of Nephrology : JASN · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

2 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

10 authors at 5 institutions in 2 countries.

V BilimDepartment of Urology, Yamagata University School of Medicine, Iida-nishi 2-2-2, Yamagata 990-9585, Japan.
A Ougolkov
K Yuuki
S Naito
H Kawazoe
A Muto
M Oya
D Billadeau
T Motoyama
Y Tomita
Yamagata University · JPYamagata University Hospital · JPKeio University · JPMayo Clinic · USNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) is highly resistant to chemotherapy because of a high apoptotic threshold. Recent evidences suggest that GSK-3beta positively regulates human pancreatic cancer and leukaemia cell survival in part through regulation of nuclear factor (NF-kappaB)-mediated expression of anti-apoptotic molecules. Our objectives were to determine the expression pattern of GSK-3beta and to assess the anti-cancer effect of GSK-3beta inhibition in RCC.

methodsImmunohistochemistry and nuclear/cytosolic fractionation were performed to determine the expression pattern of GSK-3beta in human RCCs. We used small molecule inhibitor, RNA interference, western blotting, quantitative RT-PCR, BrDU incorporation and MTS assays to study the effect of GSK-3beta inactivation on renal cancer cell proliferation and survival.

resultsWe detected aberrant nuclear accumulation of GSK-3beta in RCC cell lines and in 68 out of 74 (91.89%) human RCCs. We found that pharmacological inhibition of GSK-3 led to a decrease in proliferation and survival of renal cancer cells. We observed that inhibition of GSK-3 results in decreased expression of NF-kappaB target genes Bcl-2 and XIAP and a subsequent increase in renal cancer cell apoptosis. Moreover, we show that GSK-3 inhibitor and Docetaxel synergistically suppress proliferation and survival of renal cancer cells.

conclusionsOur results show nuclear accumulation of GSK-3beta as a new marker of human RCC, identify that GSK-3 positively regulates RCC cell survival and proliferation and suggest inhibition of GSK-3 as a new promising approach in the treatment of human renal cancer.

Indexed as

AdultAgedCarcinoma, Renal CellCell ProliferationCell SurvivalDocetaxelFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansKidney NeoplasmsMaleMiddle AgedNF-kappa BProto-Oncogene Proteins c-bcl-2TaxoidsDocetaxelGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanN-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)ureaNF-kappa BProto-Oncogene Proteins c-bcl-2TaxoidsThiazolesUreaXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID19920820
PMCPMC2795437
OpenAlexW1997546539

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.