Abstract
Cordycepin, a bioactive compound extracted from Cordyceps sinensis, can induce apoptosis in human OEC-M1 oral cancer cells. However, the exact mechanism is still unclear. The present study aimed to investigate the underlying mechanism of cordycepin-induced apoptosis in OEC-M1 cells. Following treatment with cordycepin, apoptosis was examined and quantified using a DNA laddering assay and a cytokeratin 18 fragment enzyme-linked immunosorbent assay, respectively. Expressions of mitogen-activated protein kinases (MAPKs) and apoptosis-related proteins were detected by the western blot analysis. Our results show that a pan-caspase inhibitor, Z-VAD-FMK, could significantly inhibit cordycepin-induced apoptosis in OEC-M1 cells. In addition, treatment with cordycepin not only activated caspase-8, caspase-9, and caspase-3 but also induced Bid and poly ADP-ribose polymerase cleavages. Furthermore, cordycepin also induced the activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase, and p38 MAPKs. Among MAPKs, activation of JNK solely contributed to cordycepin-induced apoptosis with the activation of caspase-8, caspase-9, and caspase-3 and cleavage of PARP. Taken together, the present study demonstrated that cordycepin activated JNK and caspase pathways to induce apoptosis in OEC-M1 cells.
Funding Information
  • Shu-Zen Junior College of Medicine and Management (SZPT10800008, SZPT10902009, SZPT11002012, MOST-107-2320-B-471-001, MOST-109-2314-B-218-001, MOST-110-2314-B-218-001-MY2, MOST-110-2320-B-006-025-MY3, CLFHR11025, CLFHR11120)
  • Ministry of Science and Technology of the People's Republic of China (SZPT10800008, SZPT10902009, SZPT11002012, MOST-107-2320-B-471-001, MOST-109-2314-B-218-001, MOST-110-2314-B-218-001-MY2, MOST-110-2320-B-006-025-MY3, CLFHR11025, CLFHR11120)
  • Chi-Mei Medical Center, Liouying (SZPT10800008, SZPT10902009, SZPT11002012, MOST-107-2320-B-471-001, MOST-109-2314-B-218-001, MOST-110-2314-B-218-001-MY2, MOST-110-2320-B-006-025-MY3, CLFHR11025, CLFHR11120)

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