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Updated: Jul 28, 2025
Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Methylseleninic acid induces apoptosis of human bladder cancer cells through the ROS-mediated mitochondrial pathway
Yi Chen1, Yan Zhang1, Xinsheng Wang2
1Key Laboratory of Food Nutrition and Safety, Ministry of Education, College of Food Science and Engineering, Tianjin University of Science and Technology, Tianjin, China.
Abstract:
As the most common selenium derivative, methylseleninic acid (MSA) has attracted wide attention. Its apoptotic induction ability and the possible molecular mechanism in human bladder cancer (BC) J82 and T24 cells were investigated in the present study. We found that the survival of J82 and T24 cells were inhibited in a dose-dependent manner after MSA treatment. Propidium iodide (PI) staining and Annexin V-fluorescein isothiocyanate/PI double staining clarified that MSA stocked cells at G2 /M phase and caused apoptosis in J82 and T24 cells. Further, typical morphological features of apoptotic cells were also observed. Accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential were also detected by dichlorodihydrofluorescein diacetate and Rhodamin123 staining. Meanwhile, pretreatment with N-acetylcysteine, an ROS scavenging agent, found that the apoptosis of BC cells induced by MSA was related to the production of ROS. Western blot analysis results showed that MSA interrupted Bax/Bcl-2 balance, stimulated cytochrome c release into the cytoplasm, activated caspase-9 and caspase-3, and finally induced the apoptosis of the BC cells. These findings demonstrated that MSA was able to induce apoptosis in J82 and T24 cells through ROS-mediated mitochondrial apoptosis.
Insights
Methylseleninic acid (MSA) effectively inhibits human bladder cancer cell survival by inducing apoptosis. This process involves reactive oxygen species (ROS) generation and mitochondrial pathway activation.
Area of Science:
- Oncology
- Biochemistry
- Cell Biology
Background:
- Methylseleninic acid (MSA) is a common selenium derivative with potential anti-cancer properties.
- Bladder cancer (BC) remains a significant health concern, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the ability of MSA to induce apoptosis in human bladder cancer cell lines (J82 and T24).
- To elucidate the molecular mechanisms underlying MSA-induced apoptosis in these cells.
Main Methods:
- Cell viability assays, Propidium iodide (PI) staining, and Annexin V-FITC/PI double staining were used to assess cell death and cell cycle arrest.
- Reactive oxygen species (ROS) accumulation and mitochondrial membrane potential were measured.
- Western blot analysis was performed to examine key apoptosis-related proteins.
Main Results:
- MSA treatment inhibited J82 and T24 cell survival in a dose-dependent manner.
- MSA induced G2/M phase arrest and apoptosis, characterized by morphological changes.
- MSA treatment led to ROS accumulation and loss of mitochondrial membrane potential.
- N-acetylcysteine pretreatment attenuated MSA-induced apoptosis, confirming the role of ROS.
- Western blot revealed that MSA disrupted the Bax/Bcl-2 balance, promoted cytochrome c release, and activated caspase-9 and caspase-3.
Conclusions:
- MSA effectively induces apoptosis in human bladder cancer cells (J82 and T24).
- The mechanism involves ROS generation, mitochondrial pathway activation, and subsequent caspase cascade.
- MSA demonstrates potential as a therapeutic agent for bladder cancer.
