Evidence map›Paper›PMID 24842953›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014

Prostate tumor growth is impaired by CtBP1 depletion in high-fat diet-fed mice.

Cristian P Moiola, Paola De Luca, Florencia Zalazar, Javier Cotignola, Santiago A Rodríguez-Seguí, Kevin Gardner, Roberto Meiss, Pablo Vallecorsa, Omar Pignataro, Osvaldo Mazza and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 79 citations in OpenAlex.

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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

12 authors at 6 institutions in 2 countries.

Cristian P MoiolaLaboratorio de Oncología Molecular y Nuevos Blancos Terapéuticos, IBYME-CONICET; Laboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Paola De LucaLaboratorio de Oncología Molecular y Nuevos Blancos Terapéuticos, IBYME-CONICET; Laboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Florencia ZalazarLaboratorio de Oncología Molecular y Nuevos Blancos Terapéuticos, IBYME-CONICET; Laboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Javier CotignolaLaboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Santiago A Rodríguez-SeguíDepartamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), and Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET;
Kevin GardnerLaboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Roberto MeissDepartamento de Patología, Instituto de Estudios Oncológicos, Academia Nacional de Medicina;
Pablo VallecorsaDepartamento de Patología, Instituto de Estudios Oncológicos, Academia Nacional de Medicina;
Omar PignataroLaboratorio de Endocrinología Molecular y Transducción de Señales, IBYME-CONICET, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Osvaldo MazzaHospital de Clínicas "José de San Martín", Buenos Aires, Argentina; and.
Elba S VazquezLaboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET;
Adriana De SierviLaboratorio de Oncología Molecular y Nuevos Blancos Terapéuticos, IBYME-CONICET; Laboratorio de Inflamación y Cáncer, Departamento de Química Biologica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN - CONICET; adesiervi@qb.fcen.uba.ar.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARAcademia Nacional de Medicina · ARFundación Ciencias Exactas y Naturales · ARUniversity of Buenos Aires · ARHospital de Clínicas "José de San Martín" · ARNational Institutes of Health · US

Funding

Molecular linkages between epigenetic regulation and metabolism in breast cancerZIABC010847 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GARDNER, KEVIN · 2009 to 2017
$7.7M
Mechanisms of Transcriptional Control by p300ZIABC010846 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GARDNER, KEVIN · 2009 to 2017
$4.8M
Intramural NIH HHS ZIA BC010846Intramural NIH HHS ZIA BC010847
6 · The paper itself

Abstract

purposeClinical and epidemiologic data suggest that obesity is associated with more aggressive forms of prostate cancer, poor prognosis, and increased mortality. C-terminal-binding protein 1 (CtBP1) is a transcription repressor of tumor suppressor genes and is activated by NADH binding. High calorie intake decreases intracellular NAD(+)/NADH ratio. The aim of this work was to assess the effect of high-fat diet (HFD) and CtBP1 expression modulation over prostate xenograft growth. EXPERIMENTAL

designWe developed a metabolic syndrome-like disease in vivo model by feeding male nude mice with HFD during 16 weeks. Control diet (CD)-fed animals were maintained at the same conditions. Mice were inoculated with PC3 cells stable transfected with shCtBP1 or control plasmids. Genome-wide expression profiles and Gene Set Enrichment Analysis (GSEA) were performed from PC3.shCtBP1 versus PC3.pGIPZ HFD-fed mice tumors.

resultsNo significant differences were observed in tumor growth on CD-fed mice; however, we found that only 60% of HFD-fed mice inoculated with CtBP1-depleted cells developed a tumor. Moreover these tumors were significantly smaller than those generated by PC3.pGIPZ control xenografts. We found 823 genes differentially expressed in shCtBP1 tumors from HFD-fed mice. GSEA from expression dataset showed that most of these genes correspond to cell adhesion, metabolic process, and cell cycle.

conclusionsMetabolic syndrome-like diseases and CtBP1 expression cooperate to induce prostate tumor growth. Hence, targeting of CtBP1 expression might be considered for prostate cancer management and therapy in the subset of patients with metabolic syndromes.

Indexed as

Alcohol OxidoreductasesAnimalsApoptosisBiomarkers, TumorBlotting, WesternCell AdhesionCell ProliferationCell Transformation, NeoplasticChromatin ImmunoprecipitationDiet, High-FatDNA-Binding ProteinsGene Expression ProfilingGonadal Steroid HormonesHumansImmunoenzyme TechniquesMaleAlcohol OxidoreductasesBiomarkers, TumorC-terminal binding proteinDNA-Binding ProteinsGonadal Steroid HormonesRNA, MessengerRNA, Small Interfering

Identifiers

PMID24842953
PMCPMC6944435
OpenAlexW2082601129

What OpenQuestion holds

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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.