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Verteporfin suppressed mitophagy via PINK1/parkin pathway in endometrial cancer

Ming-Ming Zhao1, Bo Wang1, Wen-Xi Huang2

  • 1Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University Shanghai 200011, China.

American Journal of Cancer Research
|May 10, 2024
PubMed

Insights

Verteporfin inhibits endometrial cancer (EC) cell viability by damaging mitochondria and increasing reactive oxygen species (ROS), which suppresses mitophagy. This suggests verteporfin as a potential EC therapeutic agent.

Area of Science:

  • Oncology
  • Cell Biology
  • Mitochondrial Research

Background:

  • Endometrial cancer (EC) is a significant global health concern for women.
  • Understanding EC cell biology is crucial for developing effective treatments.
  • Targeting cellular processes like mitophagy offers potential therapeutic strategies.

Purpose of the Study:

  • To investigate the inhibitory effect of verteporfin on endometrial cancer (EC) cells.
  • To explore the mechanisms underlying verteporfin's action, particularly its impact on mitochondria and mitophagy.
  • To assess the potential of verteporfin as a therapeutic option for EC.

Main Methods:

  • Treatment of EC cells with verteporfin.
  • Assessment of mitochondrial membrane potential and reactive oxygen species (ROS) levels.
  • Analysis of cell proliferation, migration, and apoptosis.
  • Evaluation of mitophagy-related protein expression (PINK1/parkin, TOM20).
  • Rescue experiments using a ROS inhibitor (N-Acetyl Cysteine).

Main Results:

  • Verteporfin damages EC cell mitochondria, decreasing membrane potential and increasing ROS.
  • Verteporfin inhibits EC cell proliferation and migration while promoting apoptosis.
  • Verteporfin reduces the expression of mitophagy proteins PINK1/parkin and TOM20.
  • N-Acetyl Cysteine reversed the impact of verteporfin on PINK1/parkin expression, indicating ROS mediation.

Conclusions:

  • Verteporfin inhibits EC cell viability, likely by increasing ROS levels and suppressing mitophagy.
  • The observed effects suggest verteporfin's potential as a novel therapeutic agent for endometrial cancer.
  • Further research into verteporfin's anti-mitophagy effects is warranted for EC treatment development.
Keywords:
Endometrial cancerPINK1/parkin pathwaymitophagyverteporfin

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