Evidence map›Paper›PMID 16652143›Full record

ArticleOncogene2006

Novel role of Stat1 in the development of docetaxel resistance in prostate tumor cells.

S G Patterson, S Wei, X Chen, D A Sallman, D L Gilvary, B Zhong, J Pow-Sang, T Yeatman, J Y Djeu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

67 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
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  6. The role and function of CLU in cancer biology and therapy.Clinical and experimental medicine · 2023
    Review
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  20. Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article

7 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

9 authors at 3 institutions in 2 countries.

S G PattersonDepartment of Interdisciplinary Oncology, University of South Florida College of Medicine, Tampa, FL, USA.
S Wei
X Chen
D A Sallman
D L Gilvary
B Zhong
J Pow-Sang
T Yeatman
J Y Djeu
University of South Florida · USFlorida College · USMoffitt Cancer Center · US

Funding

Role of Src kinases in NK lytic functionR01CA098080 · NCI · H. LEE MOFFITT CANCER CTR &RES INST · PI DJEU, JULIE Y · 2004 to 2008
$1.4M
Targeting active adaptors to control endothelial damageR01AI056213 · NIAID · H. LEE MOFFITT CANCER CTR &RES INST · PI WEI, SHENG · 2004 to 2008
$1.4M
NCI NIH HHS CA98080NIAID NIH HHS AI056213
6 · The paper itself

Abstract

A major obstacle for clinicians in the treatment of advanced prostate cancer is the inevitable progression to chemoresistance, especially to docetaxel. It is essential to understand the molecular events that lead to docetaxel resistance in order to identify means to prevent or interfere with chemoresistance. In initial attempts to detect these events, we analysed genomic differences between non-resistant and docetaxel-resistant prostate tumor cells and, of the genes modulated by docetaxel treatment, we observed Stat1 and clusterin gene expression heightened in the resistant phenotype. In this study, we provide biochemical and biological evidence that these two gene products are related. Stat1 and clusterin protein expression was induced upon docetaxel treatment of DU145 cells and highly overexpressed in the docetaxel-resistant DU145 cells (DU145-DR). The increase in total Stat1 corresponded to an increase in phosphorylated Stat1. Interestingly, there was no detectable difference between DU145 and DU145-DR cells expression of total Stat3 and phosphorylated Stat3. Treatment of DU145-DR cells with small interfering RNA targeted for Stat1 not only resulted in the knockdown of Stat1 expression, but it also caused the inhibition of clusterin expression. Thus, Stat1 appears to play a key role in the regulation of clusterin. Remarkably, inhibition of Stat1 or clusterin expression resulted in the re-sensitization of DU145-DR cells to docetaxel. These results offer the first evidence that Stat1, and its subsequent regulation of clusterin, are essential for docetaxel resistance in prostate cancer. Targeting this pathway could be a potential therapeutic means for intervention of docetaxel resistance.

Indexed as

Antineoplastic Agents, PhytogenicBase SequenceCell LineClusterinDNA PrimersDocetaxelDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleRNA, Small InterferingSTAT1 Transcription FactorTaxoidsAntineoplastic Agents, PhytogenicClusterinDNA PrimersDocetaxelRNA, Small InterferingSTAT1 Transcription FactorTaxoids

Identifiers

PMID16652143
OpenAlexW2155317973

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.