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Updated: Mar 24, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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Goniothalamin induces apoptosis associated with autophagy activation through MAPK signaling in SK-BR-3 cells

Sukanda Innajak1, Wilawan Mahabusrakum2, Ramida Watanapokasin1

  • 1Department of Biochemistry, Faculty of Medicine, Srinakharinwirot University, Bangkok 10110, Thailand.

Oncology Reports
|March 18, 2016
PubMed

Insights

Goniothalamin, a natural compound, effectively triggers programmed cell death (apoptosis) and autophagy in human breast cancer cells. This dual action suggests its potential as a novel breast cancer therapeutic agent.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Cancer Research

Background:

  • Goniothalamin is a bioactive styryl-lactone derived from plants.
  • It exhibits diverse biological activities, including potential anticancer properties.
  • Human breast cancer cell line SK-BR-3 is a relevant model for studying therapeutic efficacy.

Purpose of the Study:

  • To investigate the anticancer effects of goniothalamin on human breast cancer cells (SK-BR-3).
  • To elucidate the molecular mechanisms underlying goniothalamin-induced cell death and survival pathways.

Main Methods:

  • Cell viability assays and morphological analysis for apoptosis.
  • Mitochondrial function assessment using JC-1 staining.
  • Western blotting to analyze protein expression (Bax, Bcl-2, caspases, PARP, JNK, p38, ERK, Akt, Atg proteins, LC3).

Main Results:

  • Goniothalamin induced apoptosis, characterized by nuclear condensation, DNA fragmentation, and apoptotic bodies.
  • It caused mitochondrial dysfunction and altered the Bax/Bcl-2 ratio.
  • Goniothalamin upregulated pro-apoptotic proteins (cleaved caspase-7, -9, PARP) and downregulated anti-apoptotic Bcl-2.
  • Apoptosis was mediated by p-JNK1/2 and p-p38 upregulation and p-ERK1/2, p-Akt downregulation.
  • Autophagy was induced via upregulation of Atg7, Atg12-Atg5, and LC3II.

Conclusions:

  • Goniothalamin promotes apoptosis and induces autophagy in SK-BR-3 cells.
  • The observed effects are linked to specific signaling pathway modulations (p38, JNK, Akt).
  • Goniothalamin shows promise as a potential therapeutic candidate for breast cancer treatment.

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