Microtubule targeting chemicals are considered excellent
antitumor drugs through their binding to
tubulin, which affects the instability of microtubules resulting in arrest of
cancer cells. The present study was designed to investigate the antitumor effects of
viriditoxin (VDT) against human
prostate cancer cells. VDT, isolated from Paecilomyces variotii fungus, which was derived from the jellyfish Nemopilema nomurai, offers a new approach for controlling resistant
bacterial infections by blocking bacterial cell division
proteins. VDT produced dose-dependent cytotoxicity against human
prostate cancer cells. Treatment with VDT promoted both apoptosis and autophagy in LNCaP cells.
Annexin V/FITC staining indicated that apoptosis occurred in VDT-treated LNCaP cells.
DAPI staining revealed morphological changes in the cell nuclei indicative of mitotic catastrophe in LNCaP cells. VDT caused cell growth inhibition via G2/M phase arrest. Moreover, VDT also increased autophagic cell death in LNCaP cells by induction of several
autophagy-related proteins such as LC3 II, Atg5, Atg7 and
beclin-1 protein, which are essential for autophagy induction. These results were also confirmed by
acridine orange staining. This study indicates that VDT could potentially be effective against
prostate cancer by promoting multiple modes of growth arrest and cell death coupled with apoptosis and autophagy.