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Reactive oxygen species mediate isoalantolactone-induced apoptosis in human prostate cancer cells
Azhar Rasul1, Jun Di, Faya Martin Millimouno
1The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China.
Abstract:
Isoalantolactone, a medicinal plant-derived natural compound, is known to induce apoptosis in various cancer cell lines. However, its effect on apoptosis in prostate cancer cells has not been addressed. Thus, we examined the effects of isoalantolactone on prostate cancer cells. It was found that isoalantolactone inhibits growth of both androgen-sensitive (LNCaP) as well as androgen-independent (PC3 and DU-145) prostate cancer cells in a dose-dependent manner. Furthermore, our results indicate that isoalantolactone-induced apoptosis in prostate cancer PC3 cells is associated with the generation of ROS and dissipation of mitochondrial membrane potential (Δψm). In addition, isoalantolactone triggers apoptosis in prostate cancer cells via up-regulation of Bax, down-regulation of Bcl-2, survivin, and significant activation of caspase-3. Isoalantolactone-induced apoptosis is markedly abrogated when the cells were pretreated with N-acetylcysteine (NAC), a specific ROS inhibitor, suggesting that the apoptosis-inducing effect of isoalantolactone in prostate cancer cells is mediated by reactive oxygen species. These findings indicate that isoalantolactone induces reactive oxygen species-dependent apoptosis in prostate cancer cells via a novel mechanism involving inhibition of survivin and provide the rationale for further in vivo and preclinical investigation of isoalantolactone against human prostate cancer.
Insights
Isoalantolactone effectively inhibits prostate cancer cell growth and induces apoptosis by generating reactive oxygen species (ROS). This natural compound offers a promising avenue for novel prostate cancer therapeutics.
Area of Science:
- Natural Product Chemistry
- Cancer Biology
- Molecular Pharmacology
Background:
- Isoalantolactone is a natural compound with known anti-cancer properties.
- Its effects on prostate cancer apoptosis remain unexplored.
Purpose of the Study:
- To investigate the impact of isoalantolactone on prostate cancer cell apoptosis.
- To elucidate the underlying molecular mechanisms.
Main Methods:
- Cell viability assays on LNCaP, PC3, and DU-145 prostate cancer cell lines.
- Mitochondrial membrane potential and reactive oxygen species (ROS) generation measurements.
- Western blot analysis for apoptosis-related proteins (Bax, Bcl-2, survivin) and caspase-3 activation.
- N-acetylcysteine (NAC) pretreatment to assess ROS involvement.
Main Results:
- Isoalantolactone demonstrated dose-dependent inhibition of both androgen-sensitive and independent prostate cancer cell growth.
- Apoptosis induction in PC3 cells correlated with increased ROS and decreased mitochondrial membrane potential.
- Upregulation of Bax, downregulation of Bcl-2 and survivin, and caspase-3 activation were observed.
- N-acetylcysteine pretreatment significantly reduced isoalantolactone-induced apoptosis, confirming ROS mediation.
Conclusions:
- Isoalantolactone induces apoptosis in prostate cancer cells through a ROS-dependent pathway.
- The mechanism involves mitochondrial dysfunction and modulation of key apoptotic proteins, including survivin inhibition.
- Isoalantolactone warrants further investigation as a potential therapeutic agent for prostate cancer.
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