Evidence map›Paper›PMID 9822607›Full record

ArticleThe EMBO journal1998

Targeted downregulation of caveolin-1 is sufficient to drive cell transformation and hyperactivate the p42/44 MAP kinase cascade.

F Galbiati, D Volonte, J A Engelman, G Watanabe, R Burk, R G Pestell, M P Lisanti

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% 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

139 citing papers in PubMed, 1 synthesis or guideline pooled it, 469 citations in OpenAlex.

  1. Pooled it
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  3. Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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79 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

7 authors at 1 institution in 1 country.

F GalbiatiThe Albert Einstein Cancer Center, Microbiology and Immunology, and Epidemiology and Social Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
D Volonte
J A Engelman
G Watanabe
R Burk
R G Pestell
M P Lisanti
Albert Einstein College of Medicine · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Initiation and Maintenance In Mammary TumorigenesisR01CA075503 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 1998 to 2011
$4.6M
ANTIPROGESTINS AND ACTIVE CELL DEATH IN BREAST CANCERR01CA070897 · NCI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI EL ETREBY, M F · 1998 to 2001
$250k
NCI NIH HHS R01-CA75503NCI NIH HHS R29-CA70897NIGMS NIH HHS T32-GM07288
6 · The paper itself

Abstract

Caveolin-1 is a principal component of caveolae membranes in vivo. Caveolin-1 mRNA and protein expression are lost or reduced during cell transformation by activated oncogenes. Interestingly, the human caveolin-1 gene is localized to a suspected tumor suppressor locus (7q31.1). However, it remains unknown whether downregulation of caveolin-1 is sufficient to mediate cell transformation or tumorigenicity. Here, we employ an antisense approach to derive stable NIH 3T3 cell lines that express dramatically reduced levels of caveolin-1 but contain normal amounts of caveolin-2. NIH 3T3 cells harboring antisense caveolin-1 exhibit anchorage-independent growth, form tumors in immunodeficient mice and show hyperactivation of the p42/44 MAP kinase cascade. Importantly, transformation induced by caveolin-1 downregulation is reversed when caveolin-1 protein levels are restored to normal by loss of the caveolin-1 antisense vector. In addition, we show that in normal NIH 3T3 cells, caveolin-1 expression levels are tightly regulated by specific growth factor stimuli and cell density. Our results suggest that upregulation of caveolin-1 may be important in mediating contact inhibition and negatively regulating the activation state of the p42/44 MAP kinase cascade.

Indexed as

CaveolinsDown-Regulation3T3 CellsAnimalsBase SequenceCalcium-Calmodulin-Dependent Protein KinasesCaveolin 1Caveolin 2Cell Transformation, NeoplasticChromosomes, Human, Pair 7Culture Media, Serum-FreeDNA, AntisenseEnzyme ActivationHumansMembrane ProteinsMiceCalcium-Calmodulin-Dependent Protein KinasesCAV1 protein, humanCav1 protein, mouseCaveolin 1Caveolin 2CaveolinsCulture Media, Serum-FreeDNA, AntisenseMembrane ProteinsOligonucleotide ProbesRNA, Messenger

Identifiers

PMID9822607
PMCPMC1171009
OpenAlexW2110453766

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.