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Si bien en principio las celulas tumorales de origen epitelial se caracterizan por su alta proliferacion, la capacidad invasiva y metastasica esta relacionada con la aparicion de mecanismos de EMT por medio de la expresion de marcadores mesenquimales como a-SMA, FSP1, vimentina y desmina .
Cells lost their original features when the pathological process of EMT occurred, which induced disappeared cell contact, damaged cell polarity, and recaptured characteristics of the mesenchymal markers, such as vimentin, a-smooth muscle actin (a-SMA), and fibroblast-specific protein 1 (FSP1).
Cancer cells interact with MSCs, thereby leading to changes in MSCs' phenotype and inducing them to adopt features of CAFs such as the expression of [alpha]-SMA, FSP1 (Fibroblast-Specific Protein), or FAP (Fibroblast-Activated Protein)  or, depending on the cancer type, MSCs can further differentiate .
FAP, [alpha]-SMA, FSP1, and PDGFR are not only markers that have important role in cancer-associated fibroblasts but also essential for the proliferation of tumor cells and stimulating metastasis of tumors [17, 24].
Using the adenovirus (TGF-[beta])and our PD mice model, the double submesothelial staining for cytokeratin (+) and FSP1 (+) was positive in approximately 37% of activated fibroblasts, indicating its epithelial origin .
For immunofluorescence analysis, sections were stained with rat anti-mouse CD11b (1:100; BD Pharmingen, USA), rat anti-mouse granulocyte differentiation antigen 1 (Gr1, 1:100; BD Pharmingen, USA), rabbit anti-mouse fibroblast-specific protein-1 (FSP1, 1:100; BD Pharmingen, USA), and subsequently rhodamine-labeled secondary antibody and counterstained with 4, 6-diamidino-2-phenylindole (DAPI; Sigma, USA).
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