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Dihydromyricetin activates AMP-activated protein kinase and P38(MAPK) exerting antitumor potential in osteosarcoma

Zhiqiang Zhao1, Jun-qiang Yin1, Man-si Wu2

  • 1Department of Musculoskeletal Oncology, The First Affiliated Hospital of Sun Yat-Sen University;

Cancer Prevention Research (Philadelphia, Pa.)
|June 5, 2014
PubMed

Insights

Dihydromyricetin shows significant antitumor activity against osteosarcoma by inducing cell-cycle arrest and apoptosis. This flavonoid may offer a new therapeutic strategy for osteosarcoma patients resistant to chemotherapy.

Area of Science:

  • Biochemistry
  • Oncology
  • Pharmacology

Background:

  • Osteosarcoma often exhibits resistance to conventional chemotherapy.
  • Novel therapeutic agents are crucial for improving patient outcomes.
  • Dihydromyricetin, a flavonoid from Ampelopsis grossedentata, has a history of medicinal use.

Purpose of the Study:

  • To investigate the antitumor potential of dihydromyricetin in osteosarcoma.
  • To elucidate the underlying molecular mechanisms of its action.
  • To evaluate its efficacy and safety in vitro and in vivo.

Main Methods:

  • In vitro and in vivo studies on osteosarcoma cells.
  • Analysis of cell-cycle progression, DNA damage, and apoptosis.
  • Investigation of signaling pathways including ATM-CHK2-H2AX, AMPKα, p38(MAPK), GSK3β, and Sox2.
  • Immunohistochemical analysis of patient samples.

Main Results:

  • Dihydromyricetin induced G2-M cell-cycle arrest, DNA damage, and apoptosis in osteosarcoma cells.
  • It downregulated Sox2 expression, reducing sphere formation.
  • The compound activated AMPKα and p38(MAPK), leading to GSK3β inactivation and subsequent p21 upregulation and Sox2 downregulation.
  • Lower p-AMPK expression was observed in some post-chemotherapy patients, suggesting combination therapy benefits.

Conclusions:

  • Dihydromyricetin exhibits potent antitumor activity against osteosarcoma through multiple signaling pathways.
  • Its mechanism involves the AMPKα-GSK3β-Sox2 pathway and induction of cell-cycle arrest and apoptosis.
  • Dihydromyricetin represents a promising therapeutic candidate for osteosarcoma, potentially enhancing chemotherapy efficacy.

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