Doxorubicin induces cell cycle arrest at the G(2)/M phase and apoptosis in murine lymphocytes by increasing Fas expression and enhancing caspase activation.
Doxorubicin (DOX) is involved in the induction of DNA damage, inhibition of cell proliferation, impairment of mitochondria, and cell death. To determine the biological effects of DOX in murine lymphocytes, we analyzed cell proliferation, cell cycle status, and apoptosis in Ba/F3 and EL4 lymphoid cells. DOX treatment resulted in significant cellular morphological alteration with increased intracellular granularity and cell size. DOX inhibited cell proliferation through cell cycle arrest at the G(2)/M phase as well as by cell death. In addition, DOX treatment dramatically upregulated Fas expression and enhanced caspase activation to promote intracellular apoptotic signaling for cell death. Treatment with an agonistic antibody stimulated Fas and accelerated the cell death effects. In conclusion, we demonstrate that DOX induces cell cycle arrest and apoptosis by increased Fas expression and ultimately results in enhanced cell death.
Kim et al. (Thu,) reported a other. Doxorubicin was evaluated on Cell proliferation, cell cycle status, and apoptosis. Doxorubicin induces cell cycle arrest at the G(2)/M phase and apoptosis in murine lymphocytes by increasing Fas expression and enhancing caspase activation.