Growth inhibition by metformin in YD-38 oral cancer cells derived from Korean
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Metformin (1,1-dimethylbiguanide hydrochloride), derived from French lilac (Galega officinalis), is a first-line drug prescribed for patients with type 2 diabetes. It has been reported to have anti-cancer effects in a variety of cancer cells. However, effects of metformin on oral cancer cells have not been clearly established. The main goal of this study was to investigate the effect of metformin on cell growth and apoptosis induction in oral cancer cells derived from Korean patients. The effect of metformin on cell growth and apoptosis induction in oral cancer cells was examined by inhibition of cell growth, DNA fragmentation analysis and immunoblotting in YD-38 human oral cancer cells derived from Korean patients. Treatment with metformin induced inhibition of cell growth depending on the metformin treatment time and concentration in YD-38 human oral cancer cells. Treatment with metformin induced nuclear fragmentation in YD-38 human oral cancer cells. Metformin promoted proteolytic cleavage of procaspase-3 with an increase in the amount of cleaved caspase-3. Cleaved PARP was increased by metformin in YD-38 human oral cancer cells. Treatment of YD-38 human oral cancer cells with metformin increased the level of Bax, but it decreased the level of Bcl-2. These results suggest that metformin can induce suppression of cell growth and cell apoptosis in YD-38 human oral cancer cells derived from Korean patients.
Abstract
Metformin (1,1-dimethylbiguanide hydrochloride), derived from French lilac (Galega officinalis), is a first-line drug prescribed for patients with type 2 diabetes. It has been reported to have anti-cancer effects in a variety of cancer cells. However, effects of metformin on oral cancer cells have not been clearly established. The main goal of this study was to investigate the effect of metformin on cell growth and apoptosis induction in oral cancer cells derived from Korean patients. The effect of metformin on cell growth and apoptosis induction in oral cancer cells was examined by inhibition of cell growth, DNA fragmentation analysis and immunoblotting in YD-38 human oral cancer cells derived from Korean patients. Treatment with metformin induced inhibition of cell growth depending on the metformin treatment time and concentration in YD-38 human oral cancer cells. Treatment with metformin induced nuclear fragmentation in YD-38 human oral cancer cells. Metformin promoted proteolytic cleavage of procaspase-3 with an increase in the amount of cleaved caspase-3. Cleaved PARP was increased by metformin in YD-38 human oral cancer cells. Treatment of YD-38 human oral cancer cells with metformin increased the level of Bax, but it decreased the level of Bcl-2. These results suggest that metformin can induce suppression of cell growth and cell apoptosis in YD-38 human oral cancer cells derived from Korean patients.
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