The Fluoroquinolones Enoxacin, Moxifloxacin, andGemifloxacin Differently Influence The Growth of HumanPluripotent and Non-Pluripotent Cells

Objective: Human embryonic s tem cells (ESCs) have a greatpotential for cell therapy. However, they might give rise to tumorseven if they are differentiated before transplantation. Ithas been reported that augmenting the RNAi pathway resis tstumorigenesis. Here, we aim to compare the potential of theRNAi enhancer enoxacin and two non-RNAi enhancing fluoroquinolones,i.e., gemifloxacin and moxifloxacin, in inhibitingthe growth of undifferentiated ESCs, to provide potentiallysafer ESC-based cell therapies.Materials and Methods: The human ESC line Royan H۶ wasmaintained in DMEM/F۱۲, ۲۰% KOSR, ۱% non-essential aminoacids, ۱% ITS, ۱% L-Gln, and bFGF (۱۲.۵ ng/ml). Humandermal fibroblas ts (HDFs) were cultured in high-Glc DMEMand ۱۵% FBS. Phase-contras t imaging, Live/Dead s taining, andMTT viability assays were used to analyze the effect of enoxacin(۱۲۴ μM), gemifloxacin, and moxifloxacin (۰~۱۲۴ μM) onthe cells.Results: Based on our phase-contras t imaging, enoxacin reducedthe growth of ESCs but not of HDFs. Additionally, incontras t to enoxacin, gemifloxacin and moxifloxacin considerablyinhibited the growth of both ESCs and HDFs in differentconcentrations. Besides, MTT assays revealed that enoxacinhad an ESC-selective inhibitory effect whereas genifloxacinand moxifloxacin inhibited the viability of both cell types.These results were confirmed using Live/Dead analyses.Conclusion: The RNAi enhancer enoxacin appears to be a selectiveinhibitor of human ESCs. In contras t, gemifloxain andmoxifloxacin induced cell death in both ESCs and HDFs.

کلیدواژه ها:

Apoptosis ، Fluoroquinolone ، S tem Cell Therapy ، Teratoma ، Pluripotency