Fibroblast activation protein as a biomarker for containment of triple-negative breast cancer

Abstract Objectives The aim of this study was to investigate effect of Talabostat (a fibroblast activation protein inhibitor) on the cell viability of MDA-MB-231 cells and organoids. And the mechanism of containment of cells and organoids was also studied. Methods Cell viability of cells was demonstrated through some assays, including CCK-8, Transwell, etc. Potential mechanisms were investigated through TEM, TUNEL staining, western blot and flow cytometry. Results It was found that the cell viability and migration of MDA-MB-231 cells were inhibited by Talabostat (one kind of FAP inhibitor). And the mitochondria-mediated apoptosis induced by Talabostat was considered as the proliferation suppression mechanism, which was certified by RNA sequencing results. More importantly, the proliferation inhibitions of organoids induced by Talabostat were realized, which suggests the repression of FAP for TNBC treatment has strong clinical values. Conclusions Herein, the therapy effect of Talabostat on triple-negative breast cancer was investigated systematically, and it was found that the cell viability and migration of MDA-MB-231 cells were inhibited by Talabostat. And the mitochondria-mediated apoptosis induced by Talabostat was considered as the proliferation suppression mechanism, which was certified by RNA sequencing results. Importantly, the proliferation inhibitions of organoids induced by Talabostat were realized, which suggests the repression of FAP for TNBC treatment has strong clinical values. Our findings shed new lights on the promising treatment strategies for TNBC.