Cordycepin induces apoptosis of human acute monocytic leukemia cells via downregulation of the ERK/Akt signaling pathway
Affiliations: Department of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University Medical School, Shanghai 200011, P.R. China, Institute of Hematology, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China, Department of Ultrasound, Renji Hospital, Shanghai Jiaotong University Medical School, Shanghai 200127, P.R. China
- Published online on: July 31, 2017 https://doi.org/10.3892/etm.2017.4855
- Pages: 3067-3073
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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The aim of the present study was to examine the apoptotic effect of cordycepin (COR) on human THP-1 acute monocytic leukemia cells. THP-1 cells were exposed to different concentrations of COR for 24, 48, 72 or 96 h. The cell viability and apoptotic rate were analyzed. The gene expression of Akt1, Akt2, Akt3, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) were assessed by reverse‑transcription quantitative PCR. Western blot analysis was used to detect the protein levels of phosphorylated (p)‑Akt, p‑extracellular signal‑regulated kinase (ERK) and cleaved caspase‑3. It was found that the viability of THP‑1 cells was inhibited by COR in a dose‑ and time‑dependent manner. After treatment with 200 µM COR for 24 h, the percentage of apoptotic cells was significantly increased. COR also downregulated the levels of Bcl‑2, Akt1, Akt2 and Akt3, and elevated the expression of Bax. The protein levels of p‑Akt and p‑ERK were suppressed and cleaved caspase‑3 was increased after treatment of COR. In conclusion, COR was found to induce apoptosis of THP‑1 acute monocytic leukemia cells through downregulation of ERK/Akt signaling.