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Caveolin-1 down-regulation and Wnt5a-containing exosome activation are required for Ha-RasV12- induced cellular transformation and mechanical phenotypes in MDCK cells
7th World Congress on Molecular Pathology
Ming-Jer Tang, Hsiu-Kuan Lin and Hsi-Hui Lin
National Cheng Kung University, Taiwan
Posters & Accepted Abstracts: J Clin Exp Pathol
Abstract
Our previous study demonstrated that cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1 (Cav1), which is suppressed in many tumor cells and in oncogene-transformed cells, is linked to regulate the mechanical phenotype. Cav1-upregulated RhoA activity and Y397FAK phosphorylation direct actin cap formation, which is positively correlated with cell elasticity and stiffness sensing in fibroblast. Ha-RasV12-induced transformation and changes in the mechanical phenotypes were reversed by re-expression of caveolin-1 and mimicked by the suppression of Cav1 in normal fibroblasts. However, the loss of Cav1 per se is necessary but not sufficient to causally drive changes in the mechanical phenotype and transformation in normal epithelial cells. In this study, we found that medium conditioned by Ha-RasV12-overexpressed MK4 cells induced cell softening, loss of stiffness sensing and increase in migration and invasion ability only in Cav1-knockdown MDCK (MDCK/shCav1) cells. Ha-RasV12-activated exosomes caused cell scattering and softening in MDCK/shCav1 cells similar to Ha- RasV12-activated conditioned medium. Wnt5a, one of the Ha-RasV12-increased exosomal proteins, also induced cell scattering and cell softening in MDCK/shCav1 cells. Suppression of Wnt5a expression and secretion by C59, a porcupine (O-acyltransferase) inhibitor or by Wnt5a siRNA inhibited Ha-RasV12-induced changes in mechanical phenotype and transformation in MK4 cells. In addition, the potency of Ha-RasV12-activated exosomes to induce cell scattering, cell softening and increase in migration and invasion ability in MDCK/shCav1 cells was blocked by the depletion of Wnt5a in MK4 cells. Taken together, these results suggested that both caveolin-1 down regulation and exosomes activation are required for Ha-RasV12-induced cellular transformation in MDCK cells. This study highlights the role of caveolin-1 in the regulation of epithelial cell responsiveness to tumor exosome-induced transformation.Biography
Ming-Jer Tang is a distinguished professor from the Department of Physiology at National Cheng Kung University Medical College, Taiwan. His research expertise includes Physiology, Cell and Molecular Biology, Tissue Engineering and Mechanobiology.
Email: mjtang1@mail.ncku.edu.tw
