XXXX sensitizes @entity788 cells to the CTLs antitumor  response induced by BCG-stimulated dendritic cells via  a  Fas-dependent pathway.

@entity1 @entity788 @entity137 @entity5 @entity4404 @entity14113 @entity10762 @entity136
BACKGROUND/OBJECTIVES: There are increasing evidences suggesting that chemotherapeutic agents can enhance the cytotoxic T lymphocytes (CTLs) antitumor effect, but the precise mechanism is not fully explained. This study aims to investigate whether @entity136 ( @entity14113 ) can sensitize @entity788 cells to the CTLs antitumor response, and explore the potential mechanism. METHODS: Cell counting kit-8 assays (CCK-8) were performed to determine the @entity5 cell proliferation. Flow cytometric analysis was conducted to analyze maturation of DCs and the expression of Fas. An @entity4404 FITC Apoptosis Detection Kit was performed to detect @entity5 cell apoptosis. CytoTox 96 Nonradioactive @entity137 assays were used to determine T cell-mediated @entity5 cell lysis. RESULTS: First, it was demonstrated that Bacillus Calmette Gu  rin (BCG) could be used to induce effective CTLs antitumor response. Then, @entity14113 inhibited the growth of @entity1 cells, induced apoptosis and upregulated the Fas expression even at a low concentration. When antagonistic anti-Fas mAb ZB4 was preincubated with @entity14113 -treated @entity1 cells, the lysis induced by CTLs was reduced. Moreover, agonistic anti-Fas mAb @entity10762 induced more apoptosis of @entity14113 -treated @entity1 cells. CONCLUSION: Our results show that @entity14113 sensitizes @entity788 cells to the CTLs antitumor response, and the sensitization is associated with upregulation of Fas on @entity788 cells.
