Monensin Induces PC-3 Prostate Cancer Cell Apoptosis via ROS Production and Ca2+ Homeostasis Disruption

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Monensin is a known ionophore with potent anticancer properties, inhibiting various cancer cell growth.
• Recent studies highlight monensin's ability to induce apoptosis in cancer cells, suggesting a promising therapeutic avenue.
• The specific anticancer mechanisms of monensin against human prostate cancer remain largely unexplored.

Purpose of the Study:

• To investigate the anticancer effects of monensin on human prostate cancer cells.
• To elucidate the underlying molecular mechanisms, including cell-cycle regulation, apoptosis induction, and the role of reactive oxygen species (ROS) and calcium (Ca2+) homeostasis.

Main Methods:

• Cell viability assays were performed to assess monensin's impact on prostate cancer cell growth.
• Western blotting, cell-cycle analysis, and annexin V/propidium iodide staining were used to evaluate apoptosis and cell-cycle arrest.
• Reactive oxygen species (ROS) production and intracellular Ca2+ flux were measured to understand monensin's effects on cellular homeostasis.

Main Results:

• Monensin significantly inhibited prostate cancer cell viability in a dose-dependent manner.
• Monensin treatment induced G1 phase cell-cycle arrest and apoptosis in PC-3 cells by regulating key cell cycle and apoptosis proteins.
• Monensin triggered ROS production and disrupted Ca2+ homeostasis, which were reversed by specific inhibitors, confirming their role in monensin-induced apoptosis.

Conclusions:

• Monensin effectively induces cell-cycle arrest and apoptosis in human prostate cancer cells.
• The anticancer effects of monensin are mediated through the regulation of cell cycle and apoptosis-related proteins.
• Monensin-induced apoptosis is dependent on mitochondrial ROS production and disruption of Ca2+ homeostasis.