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Allicin affects immunoreactivity of osteosarcoma cells through lncRNA CBR3-AS1

Wenpeng Xie1, Fengjun Ma2, Luming Dou3

  • 1Department of Orthopedics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.

Heliyon
|July 1, 2024
PubMed
Abstract

Insights

Allicin enhances osteosarcoma (OS) immunoreactivity and apoptosis by targeting the CBR3-AS1/miR-145-5p/GRP78 pathway. This study provides evidence for allicin

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Osteosarcoma (OS) is a primary bone malignancy with complex immunoreactivity.
  • Understanding the molecular mechanisms underlying OS progression and immune evasion is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the impact of allicin on osteosarcoma cell immunoreactivity.
  • To elucidate the role of the long non-coding RNA (lncRNA) CBR3-AS1/miR-145-5p/GRP78 axis in allicin's mechanism of action.
  • To provide potential clinical evidence for allicin as an immunomodulatory agent in OS.

Main Methods:

  • In vitro studies using the Saos-2 human OS cell line treated with varying concentrations of allicin.
  • Transfection with CBR3-AS1 abnormal expression vectors to assess its influence on OS cells.
  • Rescue experiments to validate the regulatory relationships within the CBR3-AS1/miR-145-5p/GRP78 axis.
  • In vivo tumorigenesis experiments in nude mice to evaluate allicin's effects on tumor growth and T-lymphocyte subsets.

Main Results:

  • Allicin treatment decreased Saos-2 cell activity and increased apoptosis in a dose-dependent manner.
  • Allicin modulated the expression of key molecules: decreasing CBR3-AS1 and GRP78, while increasing miR-145-5p.
  • Silencing CBR3-AS1 mimicked allicin's effects, reducing cell activity and enhancing apoptosis, mitophagy, and endoplasmic reticulum stress.
  • Rescue experiments confirmed the regulatory axis: CBR3-AS1 influenced OS cells via miR-145-5p, and miR-145-5p's effects were mediated by GRP78.
  • In vivo studies demonstrated that allicin and the identified molecular axis regulate tumor growth, and allicin activates CD4+CD8+ T-cells, indicating enhanced immunoreactivity.

Conclusions:

  • Allicin effectively activates osteosarcoma immunoreactivity and induces apoptosis.
  • The mechanism involves the modulation of the lncRNA CBR3-AS1/miR-145-5p/GRP78 molecular axis.
  • These findings support allicin's potential as a therapeutic agent for osteosarcoma by enhancing anti-tumor immunity.
Keywords:
GRP78Immunological activityOsteosarcomaallicinlncRNA CBR3-AS1miR-145-5p

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