Bortezomib induces apoptosis and autophagy in osteosarcoma cells through mitogen-activated protein kinase pathway in

Zhiyuan Lou1, Tingting Ren, Xianbo Peng

  • 1Musculoskeletal Tumour Centre, People's Hospital, Peking University, Beijing, China.

Abstract

Insights

Bortezomib effectively inhibits osteosarcoma HOS cell growth, inducing apoptosis and autophagy. These effects are linked to changes in mitogen-activated protein kinase (MAPK) signaling pathways, suggesting bortezomib as a potential osteosarcoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Osteosarcoma is a primary bone malignancy with limited effective treatments.
  • Understanding the molecular mechanisms of novel therapeutic agents is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the anti-cancer effects of bortezomib on human osteosarcoma HOS cells.
  • To elucidate the underlying molecular mechanisms, including cell cycle changes, apoptosis, autophagy, and MAPK signaling.

Main Methods:

  • Human osteosarcoma HOS cells were treated with varying concentrations of bortezomib.
  • Cell viability, cell cycle progression, apoptosis, and autophagy were assessed using assays like annexin V-FITC and Western blotting.
  • Mitogen-activated protein kinase (MAPK) pathway activation was analyzed via Western blotting.

Main Results:

  • Bortezomib demonstrated time- and dose-dependent inhibition of HOS cell growth.
  • Bortezomib induced apoptosis and autophagy in a dose-dependent manner.
  • Changes in MAPK signaling molecules (MEK1/2, ERK1/2, JNK, p38) correlated with bortezomib-induced apoptosis and autophagy.

Conclusions:

  • Bortezomib effectively induces apoptosis and autophagy in human osteosarcoma HOS cells.
  • The study provides insights into bortezomib's mechanism of action involving MAPK pathways.
  • Bortezomib shows potential as a chemotherapeutic agent for osteosarcoma treatment.

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