JNK pathway mediates curcumin-induced apoptosis and autophagy in osteosarcoma MG63 cells

Yaowu Zhang1, Pingbo Chen1, Hangang Hong1

  • 1Department of Orthopedic Surgery, Traditional Chinese Medicine Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang 830001, P.R. China.

Insights

Curcumin induces apoptosis and autophagy in osteosarcoma cells. Autophagy may promote resistance to curcumin-induced apoptosis, offering insights for cancer treatment strategies.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Human osteosarcoma is a prevalent bone cancer in children and adolescents.
  • Curcumin is known to induce apoptosis in osteosarcoma MG63 cells via the mitochondrial pathway.
  • The interplay between curcumin-induced autophagy and apoptosis in osteosarcoma remains unclear.

Purpose of the Study:

  • To investigate if curcumin induces autophagy in osteosarcoma cells.
  • To elucidate the interaction between apoptosis and autophagy in response to curcumin.
  • To explore the role of the c-Jun N-terminal kinase (JNK) signaling pathway.

Main Methods:

  • Treatment of MG63 osteosarcoma cells with curcumin.
  • Assessment of apoptosis and autophagy induction.
  • Inhibition of apoptosis and autophagy using specific inhibitors (SP600125, 3-methyladenine).
  • Analysis of the c-Jun N-terminal kinase (JNK) signaling pathway.

Main Results:

  • Curcumin significantly induced both apoptosis and autophagy in MG63 cells.
  • Inhibiting apoptosis enhanced curcumin-induced autophagy, mediated by JNK pathway activation.
  • Inhibiting autophagy increased curcumin-induced apoptosis.
  • Autophagy appears to play a role in resistance to curcumin-induced apoptosis.

Conclusions:

  • Curcumin elicits both apoptosis and autophagy in osteosarcoma cells.
  • Autophagy may confer resistance to curcumin-induced apoptosis, potentially through JNK signaling.
  • Understanding this interaction is crucial for developing effective curcumin-based therapeutic strategies for osteosarcoma.

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