Tyrosine phosphorylation of tumor cell caveolin-1: impact on cancer progression

Caveolin-1 (CAV1) has long been implicated in cancer progression, and while widely accepted as an oncogenic protein, CAV1 also has tumor suppressor activity. CAV1 was first identified in an early study as the primary substrate of Src kinase, a potent oncoprotein, where its phosphorylation correlated...

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Bibliographic Details
Published in:Cancer and metastasis reviews 2020-06, Vol.39 (2), p.455-469
Main Authors: Wong, Timothy H., Dickson, Fiona H., Timmins, Logan R., Nabi, Ivan R.
Format: Article
Language:English
Subjects:
Animals
Biomedical and Life Sciences
Biomedicine
Cancer
Cancer Research
Caveolin
Caveolin 1 - metabolism
Caveolin-1
Cell adhesion & migration
Cell migration
Cell Movement - physiology
Development and progression
Disease Progression
Focal Adhesions - metabolism
Humans
Kinases
Metabolism
Neoplasms - metabolism
Neoplasms - pathology
Oncology
Oxidative metabolism
Oxidative stress
Phenols
Phosphorylation
Protein interaction
Src protein
src-Family Kinases - metabolism
Tumor suppressor genes
Tyrosine
Tyrosine - metabolism
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Summary:Caveolin-1 (CAV1) has long been implicated in cancer progression, and while widely accepted as an oncogenic protein, CAV1 also has tumor suppressor activity. CAV1 was first identified in an early study as the primary substrate of Src kinase, a potent oncoprotein, where its phosphorylation correlated with cellular transformation. Indeed, CAV1 phosphorylation on tyrosine-14 (Y14; pCAV1) has been associated with several cancer-associated processes such as focal adhesion dynamics, tumor cell migration and invasion, growth suppression, cancer cell metabolism, and mechanical and oxidative stress. Despite this, a clear understanding of the role of Y14-phosphorylated pCAV1 in cancer progression has not been thoroughly established. Here, we provide an overview of the role of Src-dependent phosphorylation of tumor cell CAV1 in cancer progression, focusing on pCAV1 in tumor cell migration, focal adhesion signaling and metabolism, and in the cancer cell response to stress pathways characteristic of the tumor microenvironment. We also discuss a model for Y14 phosphorylation regulation of CAV1 effector protein interactions via the caveolin scaffolding domain.
ISSN:0167-7659
1573-7233
DOI:10.1007/s10555-020-09892-9