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Updated: Jan 30, 2026

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry
Published on: September 1, 2019
Norcantharidin inhibits viability and induces cell cycle arrest and apoptosis in osteosarcoma
Yingchun Zhu1, Yunfeng Mi1, Zheyang Wang1
1Department of Orthopedics, Ningbo First Hospital, Ningbo, Zhejiang 315000, P.R. China.
Abstract:
Osteosarcoma is the most frequent malignant bone tumor in children and adolescents. Norcantharidin (NCTD) is a purified component from blister beetles and has been identified to exert antitumor effects in a variety of cancer types. However, the antitumor effect of NCTD in osteosarcoma remains to be elucidated. In the current study, it was first demonstrated that NCTD inhibited proliferation and induced G2/M-phase arrest and cell apoptosis in human osteosarcoma cells. Furthermore, NCTD significantly decreased the phosphorylation of Akt and the mammalian target of rapamycin in human osteosarcoma cells. These results suggest that NCTD is a promising candidate for the treatment of osteosarcoma patients in the future.
Insights
Norcantharidin (NCTD) shows promise for treating osteosarcoma. This study found NCTD inhibits cancer cell growth, halts cell division, and triggers cell death in osteosarcoma. NCTD may be a future treatment option.
Area of Science:
- Oncology
- Pharmacology
Background:
- Osteosarcoma is a prevalent bone cancer in pediatric and adolescent populations.
- Norcantharidin (NCTD), derived from blister beetles, exhibits known antitumor properties across various cancers.
- The specific efficacy of NCTD against osteosarcoma requires further investigation.
Purpose of the Study:
- To investigate the antitumor effects of Norcantharidin (NCTD) on human osteosarcoma cells.
- To elucidate the underlying molecular mechanisms of NCTD's action in osteosarcoma.
Main Methods:
- Treatment of human osteosarcoma cells with NCTD.
- Analysis of cell proliferation, cell cycle progression (G2/M phase), and apoptosis.
- Assessment of signaling pathways, including Akt and mammalian target of rapamycin (mTOR) phosphorylation.
Main Results:
- NCTD significantly inhibited proliferation in human osteosarcoma cells.
- NCTD induced cell cycle arrest at the G2/M phase and promoted apoptosis.
- NCTD treatment led to decreased phosphorylation of Akt and mTOR.
Conclusions:
- NCTD demonstrates significant antitumor activity against osteosarcoma cells.
- The mechanism involves inhibition of proliferation, induction of apoptosis, and modulation of the Akt/mTOR pathway.
- NCTD presents a potential therapeutic candidate for osteosarcoma treatment.
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