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Rosiglitazone induces apoptosis on human bladder cancer 5637 and T24 cell lines
Xiaoyuan Xu1, Jianjun Wang2, He Jiang1
1Key Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University Jiujiang, China.
Abstract:
Rosiglitazone is a synthetic ligand of peroxisome proliferator-activated receptor γ (PPARγ), and it can induce apoptosis and autophagy in a variety of cancer cells. In the present study, we aimed to investigate the influence of rosiglitazone on the proliferation and apoptosis of the 5637 and T24 human bladder cancer cell lines. The results demonstrated that the level of growth inhibition rate was gradually increased by treating the 5637 and T24 cells with higher doses of rosiglitazone and longer incubation time. Rosiglitazone exerted a potent inhibiting effect on migration of the 5637 and T24 cell lines. Moreover, rosiglitazone exerted a antineoplastic activity by inducing apoptosis and cell cycle arrest. Furthermore, treatment with rosiglitazone led to decrease the anti-apoptotic protein Bcl-2 level and increase the pro-apoptotic protein caspase 3 level in 5637 and T24 cells. Importantly, the protein expression of PPAR γ was significantly increased in the present of rosiglitazone in 5637 and T24 cells as compared to control group. In conclusion, the present study demonstrates that rosiglitazone has a potential antineoplastic activity in human bladder cancer cell lines, and the underlying mechanism was mediated, at least partially, through regulation of apoptosis-related protein and PPAR γ expression.
Insights
Rosiglitazone effectively inhibits human bladder cancer cell proliferation and migration. This antineoplastic effect is mediated by inducing apoptosis and cell cycle arrest, involving regulation of apoptosis-related proteins and peroxisome proliferator-activated receptor gamma (PPARγ) expression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Rosiglitazone is a peroxisome proliferator-activated receptor gamma (PPARγ) ligand known to induce apoptosis and autophagy in cancer cells.
- Bladder cancer remains a significant health concern, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the effects of rosiglitazone on human bladder cancer cell lines (5637 and T24).
- To elucidate the mechanisms underlying rosiglitazone's potential antineoplastic activity.
Main Methods:
- Treatment of 5637 and T24 cells with varying doses and incubation times of rosiglitazone.
- Assessment of cell proliferation, migration, apoptosis, and cell cycle arrest.
- Analysis of apoptosis-related protein expression (Bcl-2, caspase 3) and PPARγ levels.
Main Results:
- Rosiglitazone demonstrated dose- and time-dependent inhibition of cell proliferation and migration.
- The drug induced apoptosis and cell cycle arrest in both cell lines.
- Rosiglitazone decreased anti-apoptotic Bcl-2 and increased pro-apoptotic caspase 3 levels.
- PPARγ protein expression was significantly upregulated by rosiglitazone treatment.
Conclusions:
- Rosiglitazone exhibits potential antineoplastic activity against human bladder cancer cells.
- The mechanism involves the regulation of apoptosis-related proteins and PPARγ expression.
- Rosiglitazone represents a promising agent for further investigation in bladder cancer therapy.
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