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JNK Inactivation Induces Polyploidy and Drug-Resistance in Coronarin D-Treated Osteosarcoma Cells

Chang-Te Hsu1, Yi-Fu Huang2, Chen-Pu Hsieh3,4

  • 1Department of Orthopedic Surgery, Changhua Christian Hospital, Changhua 50006, Taiwan. 169485@cch.org.tw.

Molecules (Basel, Switzerland)
|August 26, 2018
PubMed

Insights

Coronarin D, a natural compound, inhibits osteosarcoma cell growth by inducing apoptosis and mitotic arrest. Targeting c-Jun NH2-terminal kinase (JNK) influences these processes, offering potential therapeutic strategies for osteosarcoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cancer therapy often targets proliferating cells.
  • Osteosarcoma is a challenging bone cancer with limited treatment options.
  • Natural compounds are explored for their therapeutic potential.

Purpose of the Study:

  • To investigate the effect of coronarin D on osteosarcoma cell proliferation.
  • To elucidate the molecular mechanisms underlying coronarin D's action, focusing on cell cycle regulation and apoptosis.
  • To determine the role of c-Jun NH2-terminal kinase (JNK) signaling in coronarin D's anti-cancer effects.

Main Methods:

  • Osteosarcoma cell lines (HOS) were treated with coronarin D.
  • Apoptosis was assessed via caspase-3 activation and DNA condensation.
  • Cell cycle progression was analyzed by monitoring cyclin B1 levels.
  • JNK pathway activation was measured using Western blotting.
  • JNK inhibitors were used to block JNK signaling.

Main Results:

  • Coronarin D significantly suppressed osteosarcoma cell proliferation.
  • Treatment induced apoptosis and mitotic arrest, evidenced by caspase-3 activation, cyclin B1 accumulation, and DNA condensation.
  • Coronarin D increased phosphorylated JNK levels.
  • JNK inhibition prevented mitotic arrest and apoptosis, leading to polyploidy.
  • JNK inactivation conferred resistance to coronarin D-induced cell death.

Conclusions:

  • Coronarin D exhibits anti-proliferative and pro-apoptotic effects on osteosarcoma cells.
  • JNK signaling plays a critical role in mediating coronarin D-induced mitotic arrest and apoptosis.
  • Targeting JNK in conjunction with coronarin D may represent a novel therapeutic strategy for osteosarcoma.
Keywords:
JNKcoronarin Dosteosarcoma

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