Evidence map›Paper›PMID 19372209›Full record

ArticleMolecular pharmacology2009

Thiazolidinediones mimic glucose starvation in facilitating Sp1 degradation through the up-regulation of beta-transducin repeat-containing protein.

Shuo Wei, Hsiao-Ching Chuang, Wan-Chi Tsai, Hsiao-Ching Yang, Shiuh-Rong Ho, Andrew J Paterson, Samuel K Kulp, Ching-Shih Chen

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2009. 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
1.6field-weighted citation impact, top 17% 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, 49 citations in OpenAlex.

  1. Role of post-translational modifications of Sp1 in cancer: state of the art.Frontiers in cell and developmental biology · 2024
    Review
  2. Review
  3. Review
  4. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  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

8 authors at 4 institutions in 2 countries.

Shuo WeiDivision of Medicinal Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.
Hsiao-Ching Chuang
Wan-Chi Tsai
Hsiao-Ching Yang
Shiuh-Rong Ho
Andrew J Paterson
Samuel K Kulp
Ching-Shih Chen
The Ohio State University · USFu Jen Catholic University · TWChung Shan Medical University · TWUniversity of Alabama at Birmingham · US

Funding

Targeting Akt and Bcl-2 in Prostate Cancer PreventionR01CA112250 · NCI · OHIO STATE UNIVERSITY · PI CHEN, CHING-SHIH · 2005 to 2015
$2.8M
NCI NIH HHS CA112250
6 · The paper itself

Abstract

This study investigated the mechanism by which the transcription factor Sp1 is degraded in prostate cancer cells. We recently developed a thiazolidinedione derivative, (Z)-5-(4-hydroxy-3-trifluoromethylbenzylidene)-3-(1-methylcyclohexyl)-thiazolidine-2,4-dione (OSU-CG12), that induces Sp1 degradation in a manner paralleling that of glucose starvation. Based on our finding that thiazolidinediones suppress beta-catenin and cyclin D1 by up-regulating the E3 ligase SCF(beta-TrCP), we hypothesized that beta-transducin repeat-containing protein (beta-TrCP) targets Sp1 for proteasomal degradation in response to glucose starvation or OSU-CG12. Here we show that either treatment of LNCaP cells increased specific binding of Sp1 with beta-TrCP. This direct binding was confirmed by in vitro pull-down analysis with bacterially expressed beta-TrCP. Although ectopic expression of beta-TrCP enhanced the ability of OSU-CG12 to facilitate Sp1 degradation, suppression of endogenous beta-TrCP function by a dominant-negative mutant or small interfering RNA-mediated knockdown blocked OSU-CG12-facilitated Sp1 ubiquitination and/or degradation. Sp1 contains a C-terminal conventional DSG destruction box ((727)DSGAGS(732)) that mediates beta-TrCP recognition and encompasses a glycogen synthase kinase 3beta (GSK3beta) phosphorylation motif (SXXXS). Pharmacological and molecular genetic approaches and mutational analyses indicate that extracellular signal-regulated kinase-mediated phosphorylation of Thr739 and GSK3beta-mediated phosphorylation of Ser728 and Ser732 were critical for Sp1 degradation. The ability of OSU-CG12 to mimic glucose starvation to activate beta-TrCP-mediated Sp1 degradation has translational potential to foster novel strategies for cancer therapy.

Indexed as

beta-Transducin Repeat-Containing ProteinsCell Line, TumorFemaleGlucoseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMaleMAP Kinase Kinase 1PhosphorylationProstatic NeoplasmsReceptors, AndrogenSp1 Transcription FactorThiazolidinedionesUp-Regulation5-(4-hydroxy-3-trifluoromethylbenzylidene)-3-(1-methylcyclohexyl)thiazolidine-2,4-dioneAR protein, humanbeta-Transducin Repeat-Containing ProteinsGlucoseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanMAP2K1 protein, humanMAP Kinase Kinase 1Receptors, AndrogenSp1 Transcription FactorThiazolidinediones

Identifiers

PMID19372209
PMCPMC2701453
OpenAlexW2142043048

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.