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Abstract
Previous studies have shown that 7-b (6-(dodecylamino)-2-(3-(4-methylpiperazin-1-yl)propyl)-1H-benzo-[de]isoquinoline-1,3(2H)-dione),
a novel amonafide-based DNA intercalator, was generated as a new anticancer candidate.
However, the effects induced by 7-b and the molecular mechanisms involved remain poorly
understood in Burkitt's lymphoma. To shed light on these issues, we have investigated
the effects of 7-b on proliferation, cell cycle progression, apoptosis activity and
oxidative stress levels of lymphoma Raji cells in vitro. Our results showed that 7-b
inhibited the proliferation of Raji cells and induced G1 cell cycle arrest in a dose-dependent
manner. Moreover, 7-b treatment triggered programmed cell death, production of reactive
oxygen species (ROS) and alteration of the mitochondrial membrane potential (Δψm).
Altogether our results showed that 7-b mediated its growth inhibitory effects on Raji
cells via the activation of a ROS-mediated mitochondrial pathway and cell cycle checkpoint
signaling pathway which subsequently targeted p21.