AI Article Synopsis
- Pyroptosis is a programmed cell death essential for immune response and disease, with recent studies showing chemotherapy drugs can trigger it via gasdermin E (GSDME) cleavage.
- This research focused on dioscin's effects on osteosarcoma (OS) and revealed that it causes GSDME-dependent pyroptosis and activates caspase-3.
- Dioscin also inhibits OS cell growth by inducing cell cycle arrest and apoptosis through the JNK/p38 signaling pathway, making it a possible therapeutic option for treating osteosarcoma.
Article Abstract
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.
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| http://dx.doi.org/10.1002/jcp.29197 | DOI Listing |
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