Cordycepin induces apoptosis and autophagy in human neuroblastoma SK-N-SH and BE(2)-M17 cells

Abstract

Abstract. Cordycepin, also termed 3'-deoxyadenosine, is a derivative of the nucleoside adenosine that represents a potential novel class of anticancer drugs targeting the 3' untranslated region of RNAs. Cordycepin has been reported to induce apoptosis in certain cancer cell lines, but the effects of cordycepin on human neuroblastoma cells have not been studied. In the present study, an MTT assay revealed that cordycepin inhibits the viability of neuroblastoma SK-N-SH and BE(2)-M17 cells in a dose-dependent manner. In addition, cordycepin increases the early-apoptotic cell population of SK-N-SH cells, as determined by fluorescence-activated cell sorting analysis. The induction of apoptosis in neuroblastoma cells by cordycepin was further confirmed by western blotting, which revealed cleavage of caspase-3 and poly(adenosine diphosphate-ribose) polymerase 1 in the SK-N-SH and BE(2)-M17 cells. Cordycepin also induced the formation of a punctate pattern of light-chain 3 (LC3)-associated green fluorescence in the SK-N-SH cells transfected with a pEGFP-LC3 vector. Furthermore, western blotting revealed cleavage of LC3 A/B in cordycepin-treated neuroblastoma SK-N-SH cells. Taken together, the results indicate that cordycepin significantly increases apoptosis and autophagy in neuroblastoma cells, and may therefore be a drug candidate for neuroblastoma therapy, but requires additional evaluation.

Cordycepin induces apoptosis in SGC-7901 cells through mitochondrial extrinsic phosphorylation of PI3K/Akt by generating ROS

“…To our knowledge, this is the first report showing the mechanism behind with cordycepin induced gastric cancer cell cytotoxicity. Cordycepin not only induced SGC-7901 cells growth changes but also triggers their morphology changes in line with initial reports (36,37). This is due to the unique resemblance of cordycepin to disturb the cell membranes leading to a DNA damage influencing cell death by apoptosis.…”

The critical role of quercetin in autophagy and apoptosis in HeLa cells

“…Autophagy and apoptosis are obviously different in terms of morphological or biochemical metabolic pathways, but there is a link between their functions. Due to interaction of apoptosis and autophagyrelated molecules, in some cases, autophagy and apoptosis can promote or antagonize each other [14,15]. Our results suggest that the proliferation rate of HeLa cell in 3-Ma and quercetin group is lower than that in quercetin alone group, indicating that inhibition of autophagy can increase the inhibition rate of HeLa cells.…”

Cordycepin inhibits chondrocyte hypertrophy of mesenchymal stem cells through PI3K/Bapx1 and Notch signaling pathway

“…Cordycepin has been considered as an effective antioxidative agent with protective effects on respiratory system (14), nervous system (15), endocrine system (16), and tumor metastasis (12, 17, 18). Based on the characteristics of cordycepin, we hypothesized that cordycepin might also have effect on cartilage metabolism.…”