Saponins from Rubus parvifolius L. Induce Apoptosis in Human Chronic Myeloid Leukemia Cells through AMPK Activation and STAT3 Inhibition

Ge, Yu-Qing; Xu, Xiao-Feng; Yang, Bo; Chen, Zhe; Cheng, Ru-Bin

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자료유형: 학술저널

저자정보: Ge, Yu-Qing (Zhejiang Provincial Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medical University) Xu, Xiao-Feng (Department of Hematology, Hangzhou Red Cross Hospital) Yang, Bo (College of Pharmaceutical Science, Zhejiang Chinese Medical University) Chen, Zhe (Zhejiang Provincial Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medical University) Cheng, Ru-Bin (College of Pharmaceutical Science, Zhejiang Chinese Medical University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제13호

발행연도: 2014.1

수록면: 5,455 - 5,461 (7page)

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Background: Saponins are a major active component for the traditional Chinese medicine, Rubus parvifolius L., which has shown clear antitumor activities. However, the specific effects and mechanisms of saponins of Rubus parvifolius L. (SRP) remain unclear with regard to human chronic myeloid leukemia cells. The aim of this study was to investigate inhibition of proliferation and apoptosis induction effects of SRP in K562 cells and further elucidate its regulatory mechanisms. Materials and Methods: K562 cells were treated with different concentrations of SRP and MTT assays were performed to determine cell viability. Apoptosis induction by SRP was determined with FACS and DAPI staining analysis. Western blotting was used to detect expression of apoptosis and survival related genes. Specific inhibitors were added to confirm roles of STAT3 and AMPK pathways in SRP induction of apoptosis. Results: Our results indicated that SRP exhibited obvious inhibitory effects on the growth of K562 cells, and significantly induced apoptosis. Cleavage of pro-apoptotic proteins was dramatically increased after SRP exposure. SRP treatment also increased the activities of AMPK and JNK pathways, and inhibited the phosphorylation expression level of STAT3 in K562 cells. Inhibition of the AMPK pathway blocked the activation of JNK by SRP, indicating that SRP regulated the expression of JNK dependent oon the AMPK pathway. Furthermore, inhibition of the latter significantly conferred resistance to SRP pro-apoptotic activity, suggesting involvement of the AMPK pathway in induction of apoptosis. Pretreatment with a STAT3 inhibitor also augmented SRP induced growth inhibition and cell apoptosis, further confirming roles of the STAT3 pathway after SRP treatment. Conclusions: Our results demonstrated that SRP induce cell apoptosis through AMPK activation and STAT3 inhibition in K562 cells. This suggests the possibility of further developing SRP as an alternative treatment option, or perhaps using it as adjuvant chemotherapeutic agent for chronic myeloid leukemia therapy.

#K562 cells #apoptosis induction #AMPK #STAT3 pathways #SRP

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Ge, Yu-Qing

소속기관 Zhejiang Provincial Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medical University