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Sulforaphane induces differential modulation of mitochondrial biogenesis and dynamics in normal cells and tumor cells

Mario Negrette-Guzmán1, Sara Huerta-Yepez2, Mario I Vega3

  • 1Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|December 21, 2016
PubMed

Insights

Sulforaphane (SFN) triggers cell death in prostate cancer by inducing mitochondrial biogenesis and fragmentation. This natural compound also promotes mitochondrial fusion in normal kidney cells, suggesting dual protective and therapeutic potential.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • The role of antioxidants in chemotherapy remains a subject of debate.
  • Sulforaphane (SFN) is a natural compound with potential therapeutic properties.
  • Mitochondrial dynamics are crucial in cellular processes, including cancer development and response to treatment.

Purpose of the Study:

  • To investigate the effects of sulforaphane (SFN) on mitochondrial biogenesis and dynamics in both normal kidney cells and prostate cancer cells.
  • To explore the underlying molecular mechanisms, including the involvement of Nrf2, PGC1α, HIF1α, and NRF1.
  • To evaluate the potential of SFN as an antineoplastic agent and tissue protectant.

Main Methods:

  • Treatment of kidney and prostate cancer cell lines with sulforaphane (SFN).
  • Analysis of mitochondrial biogenesis, fusion, and fragmentation.
  • Assessment of key molecular markers: nuclear factor E2-related factor-2 (Nrf2), peroxisome proliferator-activated receptor-γ co-activator-1α (PGC1α), hypoxia-inducible factor-1α (HIF1α), and nuclear respiratory factor-1 (NRF1).
  • Gene knockdown experiments targeting NRF1.

Main Results:

  • SFN induced mitochondrial biogenesis and fusion in kidney cells, suggesting a protective effect.
  • In prostate cancer cells, SFN induced cell death, accompanied by mitochondrial biogenesis and fragmentation.
  • SFN treatment led to Nrf2 stabilization, increased PGC1α, and decreased HIF1α in cancer cells, indicating a metabolic shift.
  • NRF1 knockdown attenuated SFN-induced cell death in prostate cancer cells, highlighting the role of mitochondrial biogenesis.

Conclusions:

  • Sulforaphane (SFN) exhibits differential effects on mitochondrial dynamics in normal versus cancer cells.
  • SFN demonstrates potential as an antineoplastic agent by inducing prostate cancer cell death through mitochondrial pathways.
  • SFN may protect normal tissues by modulating mitochondrial processes, supporting its potential for dual therapeutic and protective applications.
Keywords:
CancerCell deathMitochondrial biogenesisMitochondrial dynamicsNuclear factor E2-related factor 2Sulforaphane

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