Evidence map›Paper›PMID 19737975›Full record

ArticleMolecular cancer research : MCR2009

Functional analysis of secreted caveolin-1 in mouse models of prostate cancer progression.

Masami Watanabe, Guang Yang, Guangwen Cao, Salahaldin A Tahir, Koji Naruishi, Ken-Ichi Tabata, Elmoataz Abdel Fattah, Kartik Rajagopalan, Terry L Timme, Sanghee Park and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 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 18% 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, 40 citations in OpenAlex.

  1. Review
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  3. ATR Inhibition Induces CDK1-SPOP Signaling and Enhances Anti-PD-L1 Cytotoxicity in Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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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

16 authors at 2 institutions in 1 country.

Masami WatanabeScott Department of Urology, Baylor College of Medicine, Texas, USA.
Guang Yang
Guangwen Cao
Salahaldin A Tahir
Koji Naruishi
Ken-Ichi Tabata
Elmoataz Abdel Fattah
Kartik Rajagopalan
Terry L Timme
Sanghee Park
Shinji Kurosaka
Kohei Edamura
Ryuta Tanimoto
Francesco J Demayo
Alexei A Goltsov
Timothy C Thompson
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSGENIC MOUSE MODELS OF PROSTATE CANCERU01CA084296 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GREENBERG, NORMAN MICHAEL · 1999 to 2008
$7.6M
MECHANISMS OF METASTASIS IN EXPERIMENTAL PROSTATE CANCERR01CA068814 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMPSON, TIMOTHY CHARLES · 1995 to 2010
$3.0M
NCI NIH HHS 5U01 CA084296NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA068814NCI NIH HHS R01 CA68814NCI NIH HHS U01 CA084296
6 · The paper itself

Abstract

Previously, we reported that caveolin-1 (cav-1) is overexpressed in metastatic prostate cancer and that virulent prostate cancer cells secrete biologically active cav-1. We also showed that cav-1 expression leads to prosurvival activities through maintenance of activated Akt and that cav-1 is taken up by other cav-1-negative tumor cells and/or endothelial cells, leading to stimulation of angiogenic activities through PI-3-K-Akt-eNOS signaling. To analyze the functional consequences of cav-1 overexpression on the development and progression of prostate cancer in vivo, we generated PBcav-1 transgenic mice. Adult male PBcav-1 mice showed significantly increased prostatic wet weight and higher incidence of epithelial hyperplasia compared with nontransgenic littermates. Increased immunostaining for cav-1, proliferative cell nuclear antigen, P-Akt, and reduced nuclear p27(Kip1) staining occurred in PBcav-1 hyperplastic prostatic lesions. PBcav-1 mice showed increased resistance to castration-induced prostatic regression and elevated serum cav-1 levels compared with nontransgenic littermates. Intraprostatic injection of androgen-sensitive, cav-1-secreting RM-9 mouse prostate cancer cells resulted in tumors that were larger in PBcav-1 mice than in nontransgenic littermates (P = 0.04). Tail vein inoculation of RM-9 cells produced significantly more experimental lung metastases in PBcav-1 males than in nontransgenic male littermates (P = 0.001), and in cav-1(+/+) mice than in cav-1(-/-) mice (P = 0.041). Combination treatment with surgical castration and systemic cav-1 antibody dramatically reduced the number of experimental metastases. These experimental data suggest a causal association of secreted cav-1 and prostate cancer growth and progression.

Indexed as

Analysis of VarianceAndrogen-Binding ProteinAndrogensAnimalsCaveolin 1Cell Line, TumorDisease Models, AnimalDisease ProgressionLung NeoplasmsMaleMiceMice, TransgenicNeoplasm MetastasisNeoplasm TransplantationOrchiectomyPromoter Regions, GeneticAndrogen-Binding ProteinAndrogensCaveolin 1probasinProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID19737975
PMCPMC2887686
OpenAlexW2103618239

What OpenQuestion holds

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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.