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Diosgenin Glucoside Inhibits the Progression of Osteosarcoma MG-63 by Regulating the PI3K/AKT/mTOR Pathway

Siyuan Ruan1, Liuwei Gu1, Yuqi Wang1

  • 1Department of Traumatic Orthopedics, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, P.R. China.

Anti-Cancer Agents in Medicinal Chemistry
|April 20, 2023
PubMed
Abstract

Insights

Diosgenin glucoside (DG) from Trillium tschonoskii Maxim inhibits osteosarcoma cell growth, migration, and invasion. DG promotes apoptosis and cell cycle arrest via the PI3K/AKT/mTOR pathway, offering a potential anti-cancer therapeutic strategy.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Trillium tschonoskii Maxim (TTM) exhibits antitumor properties.
  • The specific antitumor mechanisms of Diosgenin glucoside (DG), a compound from TTM, remain unclear.

Purpose of the Study:

  • To investigate the anti-tumor effects of DG on osteosarcoma MG-63 cells.
  • To elucidate the molecular mechanisms underlying DG's action in osteosarcoma.

Main Methods:

  • Cell proliferation, apoptosis, and cell cycle were assessed using CCK-8, HE staining, and flow cytometry.
  • Cell migration and invasion were evaluated through wound healing and Transwell assays.
  • Molecular mechanisms were explored via immunohistochemistry, Western blot, and RT-PCR.

Main Results:

  • DG significantly inhibited osteosarcoma cell proliferation and activity.
  • DG induced apoptosis and G2 phase cell cycle arrest, while suppressing migration and invasion.
  • DG downregulated the PI3K/AKT/mTOR signaling pathway, inhibiting S6K1 and eIF4F expression.

Conclusions:

  • DG demonstrates significant anti-osteosarcoma effects by inhibiting proliferation, migration, invasion, and promoting apoptosis.
  • The PI3K/AKT/mTOR signaling pathway is implicated in DG's anti-tumor activity in osteosarcoma cells.
Keywords:
Diosgenin glucosidePI3K/AKT/mTOR pathwayanti-tumourantitumor effectsmTOR signallingosteosarcoma

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