Salvicine is a new
diterpenoid quinone substance from a natural source, specifically in a Chinese herb. It has powerful growth-controlling abilities against a broad range of human
cancer cells in both in vitro and in vivo environments. A significant inhibitory effect of
salvicine on multidrug-resistant (MDR) cells has also been discovered. Several research studies have examined the activities of
salvicine on
topoisomerase II (
Topo II) by inducing
reactive oxygen species (ROS) signaling. As opposed to the well-known
Topo II toxin
etoposide,
salvicine mostly decreases the catalytic activity with a negligible
DNA breakage effect, as revealed by several enzymatic experiments. Interestingly,
salvicine dramatically reduces lung metastatic formation in the MDA-MB-435 orthotopic
lung cancer cell line. Recent investigations have established that
salvicine is a new non-intercalative
Topo II toxin by interacting with the
ATPase domains, increasing
DNA-
Topo II interaction, and suppressing
DNA relegation and
ATP hydrolysis. In addition, investigations have revealed that
salvicine-induced ROS play a critical role in the anticancer-mediated signaling pathway, involving
Topo II suppression, DNA damage, overcoming multidrug resistance, and
tumor cell adhesion suppression, among other things. In the current study, we demonstrate the role of
salvicine in regulating the ROS signaling pathway and the DNA damage response (DDR) in suppressing the progression of
cancer cells. We depict the mechanism of action of
salvicine in suppressing the
DNA-
Topo II complex through ROS induction along with a brief discussion of the anticancer perspective of
salvicine.