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Troglitazone induced apoptosis via PPARγ activated POX-induced ROS formation in HT29 cells
Jing Wang1, XiaoWen Lv, JiePing Shi
1Chinese Academy of Sciences, Beijing, China. avaecn@gmail.com
Objective:
In order to investigate the potential mechanisms in troglitazone-induced apoptosis in HT29 cells, the effects of PPARγ and POX-induced ROS were explored.
Methods:
[3- (4, 5)-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay, Annexin V and PI staining using FACS, plasmid transfection, ROS formation detected by DCFH staining, RNA interference, RT-PCR & RT-QPCR, and Western blotting analyses were employed to investigate the apoptotic effect of troglitazone and the potential role of PPARγ pathway and POX-induced ROS formation in HT29 cells.
Results:
Troglitazone was found to inhibit the growth of HT29 cells by induction of apoptosis. During this process, mitochondria related pathways including ROS formation, POX expression and cytochrome c release increased, which were inhibited by pretreatment with GW9662, a specific antagonist of PPARγ. These results illustrated that POX upregulation and ROS formation in apoptosis induced by troglitazone was modulated in PPARγ-dependent pattern. Furthermore, the inhibition of ROS and apoptosis after POX siRNA used in troglitazone-treated HT29 cells indicated that POX be essential in the ROS formation and PPARγ-dependent apoptosis induced by troglitazone.
Conclusion:
The findings from this study showed that troglitazone-induced apoptosis was mediated by POX-induced ROS formation, at least partly, via PPARγ activation.
Insights
Troglitazone induces apoptosis in HT29 cells through a pathway involving PPARγ activation and POX-induced reactive oxygen species (ROS) formation. This mechanism highlights a potential therapeutic target for cancer treatment.
Area of Science:
- Molecular Biology
- Cell Biology
- Pharmacology
Background:
- Troglitazone, a drug with known effects on cell growth, has been observed to induce apoptosis in HT29 cells.
- The precise molecular mechanisms underlying troglitazone-induced apoptosis, particularly the roles of PPARγ and reactive oxygen species (ROS), require further elucidation.
Purpose of the Study:
- To investigate the mechanisms of troglitazone-induced apoptosis in HT29 cells.
- To explore the involvement of Peroxisome proliferator-activated receptor gamma (PPARγ) and POX-induced ROS in this process.
Main Methods:
- Utilized MTT assays, Annexin V/PI staining (FACS), and Western blotting to assess troglitazone's apoptotic effects.
- Investigated ROS formation using DCFH staining, and employed RNA interference (siRNA) targeting POX.
- Analyzed PPARγ pathway involvement through specific antagonist (GW9662) treatment and RT-PCR/RT-QPCR.
Main Results:
- Troglitazone induced apoptosis and inhibited HT29 cell growth, accompanied by increased ROS, POX expression, and cytochrome c release.
- These effects were attenuated by GW9662, indicating a PPARγ-dependent mechanism.
- POX siRNA treatment inhibited ROS formation and apoptosis in troglitazone-treated cells, confirming POX's essential role.
Conclusions:
- Troglitazone-induced apoptosis in HT29 cells is mediated by POX-induced ROS formation.
- This process is, at least partly, regulated through the activation of the PPARγ pathway.
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