Evidence map›Paper›PMID 22266466›Full record

ArticleCarcinogenesis2012

Control of stability of cyclin D1 by quinone reductase 2 in CWR22Rv1 prostate cancer cells.

Tze-chen Hsieh, Ching-Jen Yang, Chia-Yi Lin, Yong-Syu Lee, Joseph M Wu

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Stilbenes from Vine Extracts: Therapeutic Potential and Mechanisms.International journal of molecular sciences · 2025
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  9. Frontiers in pharmacology · 2021
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  14. Azoreductases in drug metabolism.British journal of pharmacology · 2017
    Review
  15. Article
  16. Role of Natural Stilbenes in the Prevention of Cancer.Oxidative medicine and cellular longevity · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. 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 2 countries.

Tze-chen HsiehDepartment of Biochemistry and Molecular Biology, New York Medical College, Room 133, Valhalla, NY 10595, USA. tze-chen_hsieh@nymc.edu
Ching-Jen Yang
Chia-Yi Lin
Yong-Syu Lee
Joseph M Wu
New York Medical College · USInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

Novel target proteins of resveratrol in chemopreventionR21CA104425 · NCI · NEW YORK MEDICAL COLLEGE · PI WU, JOSEPH M · 2004 to 2005
$280k
NCI NIH HHS R21 CA104425
6 · The paper itself

Abstract

Aberrant expression of cyclin D1, frequently observed in human malignant disorders, has been linked to the control of G(1)→S cell cycle phase transition and development and progression in carcinogenesis. Cyclin D1 level changes are partially controlled by GSK-3β-dependent phosphorylation at threonine-286 (Thr286), which targets cyclin D1 for ubiquitination and proteolytic degradation. In our continuing studies on the mechanism of prostate cancer prevention by resveratrol, focusing on the role of its recently discovered target protein, quinone reductase 2 (NQO2), we generated NQO2 knockdown CWR22Rv1 using short hairpin RNA (shRNA)-mediated gene silencing approach. We found that, compared with cells expressing NQO2 (shRNA08), NQO2 knockdown cells (shRNA25) displayed slower proliferation and G(1) phase cell accumulation. Immunoblot analyses revealed a significant decrease in phosphorylation of retinoblastoma Rb and cyclin D1 in shRNA25 compared with shRNA08. Moreover, shRNA25 cells showed a 37% decrease in chymotrypsin-like proteasome activity. An increase in AKT activity was also observed in shRNA25, supported by a ∼1.5-fold elevation in phosphorylation and ∼50% reduction/deactivation of GSK-3α/β at Ser21/9, which were accompanied by a decrease in phosphorylation of cyclin D1 at T286. NQO2 knockdown cells also showed attenuation of resveratrol-induced downregulation of cyclin D1. Our results indicate a hitherto unreported role of NQO2 in the control of AKT/GSK-3β/cyclin D1 and highlight the involvement of NQO2 in degradation of cyclin D1, as part of mechanism of chemoprevention by resveratrol.

Indexed as

Cell CycleCell Line, TumorCell ProliferationCyclin D1Gene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3HumansMalePhosphorylationProstatic NeoplasmsProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktQuinone ReductasesResveratrolRetinoblastoma ProteinRNA InterferenceCyclin D1Glycogen Synthase Kinase 3NRH - quinone oxidoreductase2Proteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktQuinone ReductasesResveratrolRetinoblastoma ProteinRNA, Small InterferingStilbenes

Identifiers

PMID22266466
PMCPMC4081641
OpenAlexW2098347876

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.