AI Article Synopsis

  • * Researchers conducted experiments on pancreatic cancer cells to investigate the role of caveolin-1 (Cav-1), finding that its expression helps revert cancer cells to a more epithelial state and enhances cell adhesion by increasing E-cadherin and beta-catenin levels.
  • * Additionally, Cav-1 reduces cell migration and invasion, improves sensitivity to chemotherapy, and markedly inhibits tumor growth in animal models, highlighting its potential as a therapeutic target in pancreatic cancer treatment.

Article Abstract

Pancreatic cancer is one of the deadliest cancers due to early rapid metastasis and chemoresistance. Recently, epithelial to mesenchymal transition (EMT) was shown to play a key role in the pathogenesis of pancreatic cancer. To understand the role of caveolin-1 (Cav-1) in EMT, we over-expressed Cav-1 in a pancreatic cancer cell line, Panc 10.05, that does not normally express Cav-1. Here, we show that Cav-1 expression in pancreatic cancer cells induces an epithelial phenotype and promotes cell-cell contact, with increased expression of plasma membrane bound E-cadherin and beta-catenin. Mechanistically, Cav-1 induces Snail downregulation and decreased activation of AKT, MAPK and TGF-beta-Smad signaling pathways. In vitro, Cav-1 expression reduces cell migration and invasion, and attenuates doxorubicin-chemoresistance of pancreatic cancer cells. Importantly, in vivo studies revealed that Cav-1 expression greatly suppresses tumor formation in a xenograft model. Most interestingly, Panc/Cav-1 tumors displayed organized nests of differentiated cells that were totally absent in control tumors. Confirming our in vitro results, these nests of differentiated cells showed reexpression of E-cadherin and beta-catenin at the cell membrane. Thus, we provide evidence that Cav-1 functions as a crucial modulator of EMT and cell differentiation in pancreatic cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266007PMC
http://dx.doi.org/10.4161/cc.10.21.17895DOI Listing

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