Cordycepin Induces Apoptosis through JNK-Mediated Caspase Activation in Human OEC-M1 Oral Cancer Cells
Open Access
- 3 October 2022
- journal article
- research article
- Published by Wiley in Evidence-Based Complementary and Alternative Medicine
- Vol. 2022, 1-10
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.Keywords
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)
This publication has 49 references indexed in Scilit:
- Role of PKC-ERK signaling in tamoxifen-induced apoptosis and tamoxifen resistance in human breast cancer cellsOncology Reports, 2012
- A DR4:tBID axis drives the p53 apoptotic response by promoting oligomerization of poised BAXThe EMBO Journal, 2012
- Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein KinasesMicrobiology and Molecular Biology Reviews, 2011
- Chemotherapy increases caspase-cleaved cytokeratin 18 in the serum of breast cancer patientsRadiology and Oncology, 2011
- Regulation of Bax by c-Jun NH2-terminal kinase and Bcl-xL in vinblastine-induced apoptosisBiochemical Pharmacology, 2009
- ERK1/2 MAP kinases in cell survival and apoptosisIUBMB Life, 2006
- Activation of c‐Jun NH2‐terminal kinase is required for gemcitabine's cytotoxic effect in human lung cancer H1299 cellsFEBS Letters, 2005
- Regulation of Bax Activation and Apoptotic Response to Microtubule-damaging Agents by p53 Transcription-dependent and -independent PathwaysJournal of Biological Chemistry, 2004
- Human Cytomegalovirus Causes Endothelial Injury Through the Ataxia Telangiectasia Mutant and p53 DNA Damage Signaling PathwaysCirculation Research, 2004
- AMP-activated protein kinase can induce apoptosis of insulin-producing MIN6 cells through stimulation of c-Jun-N-terminal kinaseJournal of Molecular Endocrinology, 2003