Jin-Cherng Chena, b, Yin-Ching Chanc, Juen-Haur Hwangb, d, e
a Department of Neurosurgery, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan
b School of Medicine, Tzu Chi University, Hualien, Taiwan
c Department of Food and Nutrition, Providence University, Taichung, Taiwan
d Department of Otolaryngology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan
e Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan
Abstract
Objective
Knowledge about the mechanisms underlying the cytotoxicity of tetrandrine and caffeine on glioma cells is limited. The primary objective of this study was to assess the expression of mammalian target of rapamycin (mTOR), phosphatase and tensin homolog (PTEN), histone deacetylase 1 (HDAC1), and histone acetyltransferase (p300) in RT-2 glioma cells treated with caffeine and/or tetrandrine.
Materials and methods
The cell viability and expression of mTOR, PTEN, HDAC1, and p300 in RT-2 glioma cells were assayed after treatment with caffeine and/or tetrandrine for 48 hours.
Results
The cell viability of RT-2 cells decreased significantly 48 hours after treatment with tetrandrine (5 μM) alone and tetrandrine (5 μM) combined with caffeine (0.5 mM or 1 mM), but not caffeine (0.5 mM or 1 mM) alone. The protein levels of mTOR, PTEN, and HDAC1 did not appear to change significantly after treatment with caffeine (0.5 mM or 1 mM) alone, tetrandrine (5 μM) alone, or their combinations. However, p300 increased significantly after treatment with caffeine (0.5 mM or 1 mM) alone, tetrandrine (5 μM) alone, and their combinations.
Conclusion
Tetrandrine and caffeine can increase glioma cell death additively possibly via increasing p300 expression.
Keywords
Caffeine; Glioma cells; Tetrandrine
