ArticleMolecular and cellular biology2009
The absence of caveolin-1 increases proliferation and anchorage- independent growth by a Rac-dependent, Erk-independent mechanism.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Genetic Liability for Internalizing Versus Externalizing Behavior Manifests in the Developing and Adult Hippocampus: Insight From a Meta-analysis of Transcriptional Profiling Studies in a Selectively Bred Rat Model.Biological psychiatry · 2021Pooled it
- Loss of Gαq reshapes fibroblast traits and drives tumor-stroma remodeling in oral cancer progression.EMBO reports · 2026Article
- Identification and validation of a prognostic risk model based on caveolin family genes for breastFrontiers in cell and developmental biology · 2022Article
- Neuroblastoma signalling models unveil combination therapies targeting feedback-mediated resistance.PLoS computational biology · 2021Article
- Derivation of stable embryonic stem cell-like, but transcriptionally heterogenous, induced pluripotent stem cells from non-permissive mouse strains.Mammalian genome : official journal of the International Mammalian Genome Society · 2020Article
- The mechano-sensitive response of β1 integrin promotes SRC-positive late endosome recycling and activation of Yes-associated protein.The Journal of biological chemistry · 2020Article
- Naegleria fowleri: differential genetic expression following treatment with Hesperidin conjugated with silver nanoparticles using RNA-Seq.Parasitology research · 2020Article
- The importance of caveolins and caveolae to dermatology: Lessons from the caves and beyond.Experimental dermatology · 2020Review
- Collective cancer invasion forms an integrin-dependent radioresistant niche.The Journal of experimental medicine · 2020Article
- Molecular regulation and clinical significance of caveolin-1 methylation in chronic lung diseases.Clinical and translational medicine · 2020Review
- Article
- Caveolin-1 in skin aging - From innocent bystander to major contributor.Ageing research reviews · 2019Review
- Chemotherapy induced PRL3 expression promotes cancer growth via plasma membrane remodeling and specific alterations of caveolae-associated signaling.Cell communication and signaling : CCS · 2018Article
- Caveolin-1 Inhibits Proliferation, Migration, and Invasion of Human Colorectal Cancer Cells by Suppressing Phosphorylation of Epidermal Growth Factor Receptor.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Article
- Epigenetic Regulation of Caveolin-1 Gene Expression in Lung Fibroblasts.American journal of respiratory cell and molecular biology · 2017Article
- Targeting folate receptor alpha for cancer treatment.Oncotarget · 2016Review
- Caveolin-1 regulates corneal wound healing by modulating Kir4.1 activity.American journal of physiology. Cell physiology · 2016Article
- Caveolin-1 regulates cancer cell metabolism via scavenging Nrf2 and suppressing MnSOD-driven glycolysis.Oncotarget · 2016Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Anchorage-independent growth (AIG) of cancer cells requires escape from integrin-mediated signals. A protein frequently downregulated in cancer, caveolin-1 (Cav1), mediates integrin control of several growth-regulatory pathways. We report that loss of Cav1 results in faster exit from quiescence and progress through the cell cycle, proliferation without anchorage to substrate, and absence of cyclin D1 downregulation upon serum deprivation or detachment. Surprisingly, this proliferative advantage is independent of Erk-mitogen-activated protein kinase signaling; instead, cyclin expression and cell cycle progression in the absence of Cav1 are driven by increased membrane order and Rac targeting. AIG was induced in Cav1-expressing cells by forced membrane targeting of Rac1 or by inhibiting Cav1-mediated internalization of plasma membrane ordered domains at which Rac1 accumulates. Restoring Rho activity, which is downregulated after loss of Cav1, antagonizes Rac1 and prevents cyclin D1 accumulation after serum starvation or loss of adhesion. Anchorage independence and increased proliferation in Cav1-deficient tumoral and null cells are thus due to an increased fraction of active Rac1 at membrane ordered domains. These results provide insight into the mechanisms regulating growth of cancer cells, which frequently lose Cav1 function.
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Registered trials
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.