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Narciclasine triggers apoptosis in osteosarcoma cells via JNK-mediated extrinsic and intrinsic pathways

Jia-Sin Yang1,2, Chia-Hsuan Chou1,2, Pei-Ni Chen1,2

  • 1Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.

International Journal of Medical Sciences
|March 9, 2026
PubMed

Insights

Narciclasine triggers programmed cell death (apoptosis) in osteosarcoma cells by activating the JNK signaling pathway. This natural compound also causes cell cycle arrest, offering potential for new bone cancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Osteosarcoma is a prevalent bone cancer in teenagers with a poor prognosis.
  • Narciclasine is known to induce apoptosis in various cancer types, but its effect on osteosarcoma is not well understood.

Purpose of the Study:

  • To investigate the apoptotic effects of narciclasine on human osteosarcoma cells (U2OS and HOS).
  • To elucidate the signaling pathways involved in narciclasine-induced apoptosis in osteosarcoma.

Main Methods:

  • Cell treatment with narciclasine.
  • Cell cycle analysis (sub-G1 phase).
  • Apoptosis assays (Human apoptosis array, Western blot for caspases and PARP).
  • Kinase activation analysis (ERK, JNK, p38 phosphorylation).
  • Inhibitor studies (JNK, ERK, p38 inhibitors).

Main Results:

  • Narciclasine induced dose-dependent apoptosis and sub-G1 cell cycle arrest in osteosarcoma cells.
  • Expression of apoptosis inhibitors (cIAP-1, survivin) decreased, while cleaved caspases (8, 9, 3) and PARP increased.
  • Narciclasine activated ERK, JNK, and p38 pathways.
  • JNK inhibition blocked narciclasine-induced apoptosis, while ERK and p38 inhibition had no effect.

Conclusions:

  • Narciclasine effectively induces apoptosis in human osteosarcoma cells.
  • JNK signaling plays a crucial role in mediating both extrinsic and intrinsic apoptotic pathways triggered by narciclasine in osteosarcoma.
Keywords:
JNK pathwayapoptosiscaspasenarciclasineosteosarcoma

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