Ciprofloxacin decreases survival in HT‐29 cells via the induction of TGF‐β1 secretion and enhances the anti‐proliferative effect of 5‐fluorouracil

摘要: Background and purpose:  Fluoroquinolones are potent anti-microbial agents with multiple effects on host cells tissues. Previous studies have highlighted their pro-apoptotic effect human cancer an immunoregulatory role in animal models of inflammatory bowel disease. We examined the ciprofloxacin proliferation, cell cycle apoptosis HT-29 cells, a colonic epithelial line sensitive to transforming growth factor (TGF)-β1-mediated inhibition its TGF-β1 production. also proliferation combination 5-fluorouracil (5-FU), well-established agent. Experimental approach:  Using subconfluent cultures Caco-2 we studied ciprofloxacin, 5-FU apoptosis, necrosis cycle. The mRNA expression production was RNA extracts culture supernatants respectively, using confluent cultures. Key results:  Ciprofloxacin decreased concentration- time-dependent manner. This mediated by accumulation into S-phase but without any or necrosis. Additionally, enhanced antiproliferative 5-FU. Interestingly, found up-regulate anti-proliferative abolished when blocked. Confirming this mechanism further, had no Caco-2, that lacks functional receptors. Conclusions implications:  demonstrate novel intestinal via TGF-β1.