Caveolin-1 controls mitochondrial damage and ROS production . . . Here we show that knockdown of the membrane-inserted scaffolding and structural protein caveolin-1 (Cav-1) and expression of tyrosine 14 phospho-defective Cav-1 mutant (Y14F), as opposed to phospho-mimicking Y14D, altered mitochondrial morphology, and increased mitochondrial matrix mixing, mitochondrial fusion and fission dynamics as well as
Mitochondrial Dysfunction and the Glycolytic Switch Induced . . . Here, we show that CAV1 expression increased glycolysis rates, while mitochondrial respiration was reduced by inhibition of the mitochondrial complex IV These effects correlated with increased reactive oxygen species (ROS) levels that favored CAV1-induced migration and invasion
Caveolae, caveolins, and cavins: complex control of cellular . . . Loss of Cav-1 leads to persistent eNOS activation and high levels of NO in cells through the loss of Cav-1 inhibitory effect on eNOS The Cav-1 eNOS interaction tonically inhibits eNOS activity resulting in sequestering of eNOS in caveolae and reduced NO production
Caveolin-1 controls mitochondrial damage and ROS production . . . Cav-1 expression may thus also affect cancer cell proliferation by modulating mitochondrial fusion and fission dynamics required for cell cycle progression The close interaction between cancer cells and their microenvironment is also enormously influential on cancer cell survival
Caveolin-1 promotes mitochondrial health and limits . . . We report that CRISPR Cas9 knockout (KO) of CAV1 increases mitochondrial oxidative phosphorylation, increases mitochondrial potential, and reduces ROS in MDA-MB-231 triple-negative breast cancer cells