Evidence map›Paper›PMID 23280667›Full record

ArticleInternational journal of cancer2013

Caveolin-1 is a novel regulator of K-RAS-dependent migration in colon carcinogenesis.

Upal K Basu Roy, Rebecca S Henkhaus, Fotios Loupakis, Chiara Cremolini, Eugene W Gerner, Natalia A Ignatenko

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

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  20. Endocytosis and cancer.Cold Spring Harbor perspectives in biology · 2013
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Upal K Basu RoyDepartment of Biochemistry and Molecular Biophysics, Biochemistry and Molecular and Cellular Biology Graduate Program, University of Arizona, Tucson, AZ, USA.
Rebecca S Henkhaus
Fotios Loupakis
Chiara Cremolini
Eugene W Gerner
Natalia A Ignatenko
University of Arizona · USAzienda Ospedaliera Universitaria Pisana · ITUniversity of Arizona Cancer Center

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
Role of Kallikrein 6 expression and secretion in colon cancerR01CA157595 · NCI · UNIVERSITY OF ARIZONA · PI IGNATENKO, NATALIA A · 2012 to 2016
$1.7M
Prevention of APC-Dependent Intestinal CarcinogenesisR01CA123065 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2007 to 2011
$1.6M
NCI NIH HHS CA095060NCI NIH HHS CA123065NCI NIH HHS P30 CA023074NCI NIH HHS P50 CA095060NCI NIH HHS R01 CA123065NCI NIH HHS R01 CA157595
6 · The paper itself

Abstract

Caveolin-1 is an essential component of membrane caveolae. It is an important regulator of cellular processes such as signal transduction and endocytosis. We report here, for the first time, that caveolin-1 is a target of the K-RAS oncogene in colon carcinogenesis. Caveolin-1 is induced in colon cancer cells and in human colon tumor samples, in response to K-RAS activating mutations. An activated K-RAS oncogene transcriptionally induces caveolin-1 expression in human colon cancer cells and this effect is not restricted to the type of activating K-RAS mutation. Inhibition of the P-I3 Kinase-AKT pathway, but not the ERK MAPK pathway, both important K-RAS effectors, leads to a decrease in caveolin-1 expression indicating that the AKT pathway is involved in caveolin-1 expression in response to an activated K-RAS. Increased AKT signaling induces caveolin-1 expression by increasing the activity of the transcription factor, Sp1. Interestingly; caveolin-1 depletion alters K-RAS-dependent signaling by decreasing Grb2-SOS activity. Consistent with these finding, caveolin-1-depleted cells shows decreased migration in vitro. However, caveolin-1 overexpression by itself does not increase migration whereas an activated Src can increase migration in a caveolin-1-dependent manner. This increased migration is highly dependent on the RhoA GTPase, indicating that an activated K-RAS modulates migration in part via caveolin-1 induction, and increasing RhoA activity via phospho-caveolin-1. Our findings indicate that K-RAS regulates both caveolin-1 expression and other factors affecting caveolin-1 functions in colon cancer-derived cell migration.

Indexed as

Cell MovementGenes, rasMutationBlotting, WesternCaveolin 1Cell Line, TumorCell Transformation, NeoplasticColonic NeoplasmsDisease ProgressionGene Expression Regulation, NeoplasticGTP PhosphohydrolasesHumansImmunohistochemistryImmunoprecipitationMAP Kinase Signaling SystemPlasmidsCAV1 protein, humanCaveolin 1GTP PhosphohydrolasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)rhoA GTP-Binding ProteinRHOA protein, humanSp1 Transcription Factor

Identifiers

PMID23280667
PMCPMC3633716
OpenAlexW1907827813

What OpenQuestion holds

Textmetadata
LicenceTDM
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.