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Induction of apoptosis by costunolide in bladder cancer cells is mediated through ROS generation and mitochondrial

Azhar Rasul1, Rui Bao, Mahadev Malhi

  • 1Dental Hospital, Jilin University, Changchun 130041, China.

Molecules (Basel, Switzerland)
|January 26, 2013
PubMed

Insights

Costunolide effectively inhibits human bladder cancer cell growth and induces apoptosis by generating reactive oxygen species (ROS). This natural compound shows promise as a novel therapeutic agent for bladder cancer treatment.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Bladder cancer treatment requires safer and more effective therapies.
  • Costunolide, a sesquiterpene lactone, exhibits known anticancer properties.

Purpose of the Study:

  • To investigate the effects of costunolide on human bladder cancer T24 cells.
  • To elucidate the mechanisms underlying costunolide's cytotoxic effects.

Main Methods:

  • T24 cells were treated with varying doses of costunolide.
  • Cell viability, apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential (Δψm), and key protein expressions (Bax, Bcl-2, survivin, caspase-3, PARP) were analyzed.
  • N-acetyl-cysteine (NAC) was used to assess the role of ROS.

Main Results:

  • Costunolide dose-dependently inhibited T24 cell viability and induced apoptosis.
  • Apoptosis was linked to ROS generation and mitochondrial membrane potential disruption.
  • Costunolide modulated apoptosis-related proteins, including increased Bax and decreased Bcl-2 and survivin, with caspase-3/PARP activation.
  • ROS inhibition by NAC significantly blocked costunolide's effects.

Conclusions:

  • Costunolide demonstrates significant anticancer activity against human bladder cancer T24 cells.
  • The mechanism involves ROS generation and mitochondrial pathway activation.
  • Costunolide warrants further investigation for bladder cancer therapy.

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