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Metformin Suppresses Proliferation and Viability of Rat Pheochromocytoma Cells
Min Li1, Xiuli Jiang1, Tingwei Su1
1Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China (mainland).
Abstract:
BACKGROUND Previous studies have clearly demonstrated that metformin inhibits cell proliferation and cell growth in many types of human cancers. Increased survival rates in patients with breast and lung cancer receiving metformin have also been observed. However, the effect of metformin on pheochromocytoma cells remains unexplored. MATERIAL AND METHODS Rat pheochromocytoma cells (PC12 cells) were cultured and treated with metformin or vehicle control. Cell proliferation, cell-cycle, apoptosis, genes expression, and the signaling pathways involved were analyzed in PC12 cells. RESULTS The metformin treatment reduced cell viability and proliferation in rat pheochromocytoma PC12 cells in a dose- and time-dependent manner. Furthermore, metformin exposure led to an increased apoptosis rate and cell-cycle arrest accompanied with downregulation of Ccna2 and Ccnb2. At the molecular level, the AMPK signaling pathway was activated, whereas the mTOR and ERK1/2 signaling pathways were inhibited by metformin. CONCLUSIONS Our data suggest an antiproliferative role of metformin in pheochromocytoma development, which may provide a novel option for future cancer therapy.
Insights
Metformin, a common diabetes drug, shows antiproliferative effects on rat pheochromocytoma cells. This study reveals its potential as a novel therapeutic option for pheochromocytoma cancer treatment.
Area of Science:
- Endocrinology
- Oncology
- Pharmacology
Background:
- Metformin is known to inhibit proliferation and growth in various human cancers.
- Metformin use is associated with increased survival rates in breast and lung cancer patients.
- The impact of metformin on pheochromocytoma cells has not been previously investigated.
Purpose of the Study:
- To investigate the effect of metformin on rat pheochromocytoma (PC12) cells.
- To analyze metformin's impact on cell proliferation, cell cycle, apoptosis, gene expression, and signaling pathways in PC12 cells.
Main Methods:
- Rat pheochromocytoma PC12 cells were cultured and treated with metformin or a vehicle control.
- Analyses included cell viability, proliferation assays, cell-cycle analysis, apoptosis assessment, and gene expression profiling.
- Key signaling pathways (AMPK, mTOR, ERK1/2) were examined.
Main Results:
- Metformin significantly reduced PC12 cell viability and proliferation in a dose- and time-dependent manner.
- Metformin induced apoptosis and cell-cycle arrest, with downregulation of Ccna2 and Ccnb2.
- Metformin activated the AMPK pathway while inhibiting the mTOR and ERK1/2 pathways.
Conclusions:
- Metformin exhibits an antiproliferative effect on pheochromocytoma cells.
- These findings suggest metformin as a potential therapeutic agent for pheochromocytoma treatment.
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