https://www.selleckchem.com/pr....oducts/pf-06424439.h
The reduction of the proliferative rates was attributed to the induction of ROS triggered apoptosis which was associated with activation of Caspase-3, upregulation of Bax and suppression of Bcl-2. Voacangine induced G2/M cell cycle arrest in a dose-dependent manner. Additionally, the anticancer effects of Voacangine on oral cancer cells were exerted through the inhibition of PI3K/AKT signaling cascade. Taken all together, we conclude that Voacangine is a potent anticancer molecule and may be utilized for the development of systemic
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