Evidence map›Paper›PMID 25125658›Full record

ArticleCancer research2014

NQO1 suppresses NF-κB-p300 interaction to regulate inflammatory mediators associated with prostate tumorigenesis.

Dinesh Thapa, Peng Meng, Roble G Bedolla, Robert L Reddick, Addanki P Kumar, Rita Ghosh

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

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  17. Antioxidants (Basel, Switzerland) · 2021
    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

6 authors at 1 institution in 1 country.

Dinesh ThapaDepartment of Urology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas.
Peng MengDepartment of Urology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas.
Roble G BedollaDepartment of Urology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas.
Robert L ReddickDepartment of Pathology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. Cancer Therapy and Research Center, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Addanki P KumarDepartment of Urology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. Cancer Therapy and Research Center, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Department of Pharmacology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. Department of Molecular Medicine, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. South Texas Veterans Health Care System, San Antonio, Texas.
Rita GhoshDepartment of Urology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. Cancer Therapy and Research Center, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Department of Pharmacology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. Department of Molecular Medicine, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio Texas. ghoshr@uthscsa.edu.
South Texas Veterans Health Care System · US

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR000149 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2012 to 2013
$6.8M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthKL2TR001118 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, DOUGHERTY, DONALD M · 2013 to 2017
$3.4M
Oxidative stress in prostate cancer: Efficacy of antioxidants in Nkx3.1; Pten modR01CA149516 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GHOSH, RITA · 2010 to 2014
$1.6M
Oxidative stress and programmed death pathways: Cross talk in pancreatic cancerR01AT007448 · NCCIH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KUMAR, ADDANKI PRATAP · 2012 to 2016
$1.6M
NCATS NIH HHS KL2 TR001118NCATS NIH HHS UL1 TR000149NCATS NIH HHS UL1 TR001120NCCIH NIH HHS 1R01AT7448NCCIH NIH HHS R01 AT007448NCI NIH HHS 5R01CA149516NCI NIH HHS R01 CA149516PHS HHS PDF RP101491
6 · The paper itself

Abstract

NADPH reductase NAD(P)H: quinone oxidoreductase 1 (NQO1) is needed to maintain a cellular pool of antioxidants, and this enzyme may contribute to tumorigenesis on the basis of studies in NQO1-deficient mice. In this work, we sought deeper insights into how NQO1 contributes to prostate carcinogenesis, a setting in which oxidative stress and inflammation are established contributors to disease development and progression. In the TRAMP mouse model of prostate cancer, NQO1 was highly expressed in tumor cells. NQO1 silencing in prostate cancer cells increased levels of nuclear IKKα and NF-κB while decreasing the levels of p53, leading to interactions between NF-κB and p300 that reinforce survival signaling. Gene expression analysis revealed upregulation of a set of immune-associated transcripts associated with inflammation and tumorigenesis in cells in which NQO1 was attenuated, with IL8 confirmed functionally in cell culture as one key NQO1-supported cytokine. Notably, NQO1-silenced prostate cancer cells were more resistant to androgen deprivation. Furthermore, NQO1 inhibition increased migration, including under conditions of androgen deprivation. These results reveal a molecular link between NQO1 expression and proinflammatory cytokine signaling in prostate cancer. Furthermore, our results suggest that altering redox homeostasis through NQO1 inhibition might promote androgen-independent cell survival via opposing effects on NF-κB and p53 function.

Indexed as

CarcinogenesisCell Line, TumorGene Knockdown TechniquesHumansInflammation MediatorsInterleukin-8MaleNAD(P)H Dehydrogenase (Quinone)NF-kappa Bp300-CBP Transcription FactorsProstatic NeoplasmsProtein BindingReal-Time Polymerase Chain ReactionTumor Suppressor Protein p53Inflammation MediatorsInterleukin-8NAD(P)H Dehydrogenase (Quinone)NF-kappa BNQO1 protein, humanp300-CBP Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID25125658
PMCPMC4184940
OpenAlexW2102427015

What OpenQuestion holds

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Registered trials

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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.