Dioscin inhibits the growth of human osteosarcoma by inducing G2/M-phase arrest, apoptosis, and GSDME-dependent cell death in vitro and in vivo
| Autor: | Xianyi Cai, Lei Chen, Guangfu Peng, Fengbo Mo, Wenda Zhang, Cheng Cheng, Xianzhe Liu, Shuhua Yang, Jinglong Wang, Qiuyue Ding |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Programmed cell death Physiology p38 mitogen-activated protein kinases Clinical Biochemistry Apoptosis Bone Neoplasms Diosgenin 03 medical and health sciences 0302 clinical medicine In vivo Cell Line Tumor medicine Pyroptosis Humans Osteosarcoma Cell Death Chemistry Cell Biology Cell Cycle Checkpoints medicine.disease In vitro G2 Phase Cell Cycle Checkpoints 030104 developmental biology Receptors Estrogen 030220 oncology & carcinogenesis Cancer cell Cancer research |
| Zdroj: | Journal of cellular physiology. 235(3) |
| ISSN: | 1097-4652 |
| Popis: | Pyroptosis is a form of programmed cell death (PCD) that plays a vital role in immunity and diseases. Although it was recently reported that chemotherapy drugs can induce pyroptosis through caspase-3-dependent cleavage of gasdermin E (GSDME), the role of pyroptosis in osteosarcoma (OS) with dioscin is less understood. In this study, we explored the effects of dioscin on OS in vitro and in vivo and further elucidated the underlying molecular mechanisms and found that dioscin-triggered pyroptosis in GSDME-dependent cell death and that GSDME-N was generated by caspase-3. Furthermore, dioscin inhibited cancer cell growth by inducing G2/M arrest and apoptosis through the JNK/p38 pathway. In vivo, dioscin significantly inhibited OS proliferation. Taken together, our results demonstrate that dioscin can induce apoptosis through the JNK/p38 pathway and GSDME-dependent pyroptosis in OS, identifying it as a potential therapeutic drug for treatment of this disease. |
| Databáze: | OpenAIRE |
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