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Isoliquiritigenin inhibits the proliferation, apoptosis and migration of osteosarcoma cells

Chengjun Li1, Xing Zhou1, Chang Sun1

  • 1Department of Orthopedics, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, P.R. China.

Oncology Reports
|February 6, 2019
PubMed

Insights

Isoliquiritigenin (ISL) effectively inhibits osteosarcoma growth by reducing cell proliferation, migration, and promoting apoptosis. This natural compound shows promise as a novel therapeutic agent for osteosarcoma treatment.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Osteosarcoma survival rates have stagnated, necessitating new therapeutic strategies.
  • Isoliquiritigenin (ISL), a natural compound, exhibits anti-tumor properties in various cancers.
  • The efficacy of ISL against osteosarcoma remains largely uninvestigated.

Purpose of the Study:

  • To investigate the anti-osteosarcoma effects of Isoliquiritigenin (ISL).
  • To elucidate the mechanisms underlying ISL's action on osteosarcoma cells.

Main Methods:

  • In vitro studies using Saos-2 osteosarcoma cell line.
  • In vivo xenograft tumor models.
  • Analysis of cell proliferation, apoptosis, migration, and key protein expression (cyclin D1, p53, p21, p27, Bcl-2, Bax, MMP2, MMP9).
  • Assessment of mitochondrial function and PI3K/AKT signaling pathway.

Main Results:

  • ISL significantly inhibited Saos-2 cell proliferation and migration in vitro and reduced tumor growth in vivo.
  • ISL promoted osteosarcoma cell apoptosis by downregulating Bcl-2, upregulating Bax, and impairing mitochondrial function.
  • ISL modulated the expression of cell cycle regulators (cyclin D1, p53, p21, p27) and matrix metalloproteinases (MMP2, MMP9).
  • ISL's anti-tumor effects were linked to the PI3K/AKT signaling pathway.

Conclusions:

  • Isoliquiritigenin (ISL) demonstrates significant potential as an anti-osteosarcoma agent.
  • ISL exerts its effects by inhibiting proliferation, promoting apoptosis, and reducing migration.
  • Further investigation into the PI3K/AKT pathway's role in ISL-mediated migration inhibition is warranted.

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