Identifiers
caveolin 1
HUGO:CAV1 hgnc_id:HGNC:1527 HGNC:1527 ENTREZ:857 UNIPROT:Q03135
Maps_Modules
HMC:TUMOR_PROMOTING_INFLAMMATION
HMC:ACTIVATING_INVASION_AND_METASTASIS
Cancer Associated Fibroblasts / CAF_INHIBITION_ANTITUMOR
References
CASCADE:TGFB
PMID:20855962
Cav-1 behaves as a tumor suppressor in fibroblasts
PMID:21729786
Stroma of human breast, kidney and colon carcinoma and melanoma metastases are enriched in Cav1-expressing fibroblasts
caveolin-1 (Cav1) favors cell elongation in three-dimensional cultures and promotes Rho- and force-dependent contraction, matrix alignment, and microenvironment stiffening through regulation of p190RhoGAP. In turn, microenvironment remodeling by Cav1 fibroblasts forces cell elongation.
Cav1 expression in breast CAFs correlates with low survival
PMID:18458534; PMID:19411448
Human breast cancer-associated fibroblasts (CAFs) show caveolin-1 downregulation and RB tumor suppressor functional inactivation: Implications for the response to hormonal therapy.
PMID:26828520
CAV1 and Podoplanin are markers of fibroblast activation
PMID:17517963
Caveolin-1-deficient cells lose normal cell polarity, exhibit impaired wound healing, and have decreased Rho and increased Rac and Cdc42 GTPase activities. Directional persistency of migration is lost, and the cells show an impaired response to external directional stimuli. Both Src inactivation and p190RhoGAP knockdown restore the wild-type phenotype to caveolin-1-deficient cells, suggesting that caveolin-1 stimulates normal Rho GTP loading through inactivation of the Src-p190RhoGAP pathway. These findings highlight the importance of caveolin-1 in the establishment of cell polarity during directional migration through coordination of the signaling of Src kinase and Rho GTPases.
caveolin-1 deficiency has been implicated in the aggressiveness of breast cancer stromal fibroblasts
PMID:21051947
bone marrow-derived stromal cells from Cav-1(-/-) mice had elevated levels of miR-31
hypoxia-induced degradation of Cav-1 via HIF1 and NFKB
, a loss of stromal fibroblast Cav-1 is a biomarker for chronic hypoxia, oxidative stress and autophagy in the tumor microenvironment.
PMID:25364523; PMID:22411312; PMID:11102446
CAV1 could inhibit growth factor signaling (EGFR and TGFB) and decrease prolifiration of fibroblasts.
Cav-1 interacts with the Type I TGF-beta receptor. Additionally, Cav-1 is able to suppress TGF-beta-mediated phosphorylation of Smad-2 and subsequent downstream events.
PMID:21150282
A loss of stromal Cav-1 is sufficient to dramatically increase tumor growth.
Proteomic analysis of Cav-1 deficient fibroblasts provides evidence for the onset of a myofibroblast phenotype and mitochondrial oxidative stress.
PMID:23907124
Loss of Cav-1 in the stroma and gain of monocarboxylate transporter 4 (MCT4) expression in the stroma have been found to be involved in the progression of DCIS to IDC
PMID:22874531
TGFB treatment induces the autophagy-mediated downregulation of Cav-1 in fibroblasts.