Caveolin-1 promotes pancreatic cancer cell differentiation and restores membranous E-cadherin via suppression of the epithelial-mesenchymal transition

Mechanistic Analysis of Taxol-induced Multidrug Resistance in an Ovarian Cancer Cell Line

“…EMT is a biological and molecular process in which epithelial cells lose cell polarity and gain a fibroblastic spindle-shape morphology allowing them to infiltrate tissues and invade organs, which was regarded as one of the reasons leading to drug resistance (Paraiso et al, 2013). Then caveolin-1, which is the main constituent molecule of caveolae at cell membrane, acts as a crucial modulator of EMT (Salem et al, 2011). In this study, we noticed that caveolin-1 was overexpressed in A2780/Taxol cells.…”

Epithelial-to-mesenchymal transition (EMT) confers primary resistance to trastuzumab (Herceptin)

“…75,76 In fact, the four canonical Yamanaka pluripotency factors transcriptionally impede the EMT process: Sox2/ Oct4 suppress the EMT mediator SNAIL; c-Myc downregulates TGF β1 and TGF β receptor 2 and Klf4 induces epithelial genes, including E-cadherin. [72][73][74][75][76][77] Experiments are currently underway in our laboratory to determine whether the gain of epithelial features (e.g., E-cadherin expression) upon the silencing of EMT drivers in basal/HER2 + JIMT1 cells relates to changes in the endogenous expression of pluripotent transcription factors. Considering that bona fide mammospheres are non-adherent spherical cell clusters enriched in mammary stem/progenitor cells, it is intriguing that the steady depletion of CD44 + CD24 -/low mesenchymal cells in response to the specific knockdown of SLUG/SNAIL2 does not affect the epithelial nature of the mammospheres generated by designated as the CSC subpopulation of breast cancer cells that is enriched in tumorigenic cells.…”

Involvement of epithelial to mesenchymal transition in the development of pancreatic ductal adenocarcinoma

“…They showed that overexpressed Caveolin-1 (Cav-1) in PDAC cells resulted in increased membranous expression of E-cadherin and bcatenin, reduced cell migration and invasion, and chemosensitization to doxorubicin. In addition, Cav-1 induced downregulation of Snail expression and inactivation of EMT-inducible signal pathways such as AKT, MAPK, and TGF-b-Smad [29]. Collectively, acquisition of EMT is strongly associated with chemoresistance in PDAC cells.…”

“…By contrast, chemosensitization to 5-FU and gemcitabine was seen in MSX2-knockdown PDAC cells which showed more epithelial characteristics compared with control cells [28]. Salem et al [29] also revealed the relationship between suppression of EMT and the attenuation of chemoresistance in PDAC cells. They showed that overexpressed Caveolin-1 (Cav-1) in PDAC cells resulted in increased membranous expression of E-cadherin and bcatenin, reduced cell migration and invasion, and chemosensitization to doxorubicin.…”