Thymoquinone regulates osteosarcoma cell proliferation through the P53 signaling pathway: A network pharmacology and

Chenliang Zhou1,2, Ruiyao Wang2, Fang Liu2

  • 1Department of Orthopaedics, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.

Insights

Thymoquinone (TQ) shows promise in treating osteosarcoma (OS) by inhibiting cancer cell growth and promoting apoptosis. This study identified key molecular targets, including P53 and CYCLIN D1, for TQ

Area of Science:

  • Oncology
  • Bioinformatics
  • Pharmacology

Background:

  • Osteosarcoma (OS) presents significant treatment challenges with traditional therapies often causing adverse effects and poor outcomes.
  • The antitumor properties of thymoquinone (TQ) are recognized, but its specific molecular mechanisms against OS require further elucidation.
  • p53 gene deletion is increasingly linked to cancer development and progression, suggesting its potential role in OS.

Purpose of the Study:

  • To investigate the pharmacological targets and anti-osteosarcoma (OS) mechanisms of thymoquinone (TQ).
  • To utilize systems bioinformatics, including network pharmacology and molecular docking, to uncover TQ's anti-OS effects.
  • To identify key molecular pathways and potential therapeutic targets modulated by TQ in OS.

Main Methods:

  • Network pharmacology and molecular docking simulations were employed to analyze TQ's interactions.
  • Comprehensive screening identified 23 potential targets, with 8 core targets further analyzed.
  • Enrichment analysis was performed to understand the biological processes and pathways involved.

Main Results:

  • Preliminary in vitro studies demonstrated that TQ significantly reduces OS cell proliferation.
  • TQ was observed to effectively induce apoptosis in osteosarcoma cells.
  • Downregulation of P53 and HMOX1 protein expression was noted following TQ treatment.

Conclusions:

  • TQ exhibits anti-osteosarcoma (OS) activity through mechanisms involving apoptosis induction.
  • Key therapeutic targets, including P53 and CYCLIN D1, were identified for TQ-mediated OS treatment.
  • This study provides insights into the molecular basis of TQ's efficacy against OS.

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