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Calycosin induces apoptosis via p38‑MAPK pathway‑mediated activation of the mitochondrial apoptotic pathway in human

Wei Tian1, Zhi-Wei Wang1, Bao-Ming Yuan1

  • 1Department of Orthopedics, Affiliated Hospital of Inner Mongolia University for The Nationalities, Tongliao, Inner Mongolia 028007, P.R. China.

Molecular Medicine Reports
|September 9, 2020
PubMed

Insights

Calycosin, a phytoestrogen, inhibits osteosarcoma cell growth by inducing apoptosis. It activates the p38-MAPK pathway, leading to mitochondrial dysfunction and programmed cell death in osteosarcoma cells.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Calycosin, a phytoestrogen, exhibits anti-cancer properties by inhibiting proliferation and inducing apoptosis in various tumors.
  • Osteosarcoma cells are potential targets for calycosin's pharmacological effects, primarily through apoptosis induction.

Purpose of the Study:

  • To investigate the specific molecular mechanisms underlying calycosin-induced apoptosis in osteosarcoma cells.
  • To elucidate the role of the p38-MAPK pathway in calycosin's anti-cancer effects on osteosarcoma.

Main Methods:

  • Cell viability assessed using MTT assay.
  • Apoptosis and mitochondrial dysfunction detected by Annexin V/PI and JC-1 staining via flow cytometry.
  • Protein expression analyzed through Western blot, focusing on caspases, mitochondrial proteins, and MAPK signaling.

Main Results:

  • Calycosin reduced osteosarcoma 143B cell viability and induced apoptosis, accompanied by mitochondrial membrane potential loss.
  • Calycosin modulated apoptosis-related proteins, increasing Bax and cleaved caspases, while decreasing Bcl-2, and altered cytochrome c localization.
  • Calycosin treatment phosphorylated p38-MAPK; inhibition of p38-MAPK reversed calycosin's effects on cell viability, apoptosis, and mitochondrial function.

Conclusions:

  • Calycosin inhibits osteosarcoma 143B cell growth through the induction of intrinsic apoptosis.
  • The p38-MAPK pathway is a key regulator in calycosin-mediated apoptosis and mitochondrial dysfunction in osteosarcoma.

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