Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a potent chemopreventive and potentially cancer therapeutic agent. Since rapid metabolism limits resveratrol bioavailability, derivatives less prone to metabolic transformation are being sought and tested. We evaluated the effect of resveratrol, and its analogs (pterostilbene and 3,5,4'-trimethoxystilbene) along with tannic acid, on cell cycle and apoptosis in rat C6 and human T98G glioma cells. At concentration ranges both lower and higher than IC50 calculated based on MTT assay, all these polyphenols affected the cell cycle distribution. However, resveratrol and pterostilbene increased the percentage of the cells in S phase, while trimethoxystilbene (TMS) caused a massive accumulation of cells at the G2/M phase of the cell cycle. Tannic acid had no effect on cell cycle distribution in C6 cells, but increased the number of dead cells in both glioma cell lines. The ability to induce apoptosis by tannic acid and stilbenes was confirmed by phosphatidylserine externalization, the loss of mitochondrial membrane potential and the level of cleaved caspase-3. The apoptosis rate was most significantly increased by TMS and this was related to p53 induction. These results indicate that methoxylated stilbenes are efficient inhibitors of glioma cell proliferation and apoptosis inducers and might be considered adjuvants in glioma therapy.
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PMID:The effect of resveratrol, its naturally occurring derivatives and tannic acid on the induction of cell cycle arrest and apoptosis in rat C6 and human T98G glioma cell lines. 2859 35

Tannic acid (TA), a natural plant compound, is known to induce the death of cancer cells in various types of cancer. The present study was designed with the aim of exploring the effects of tannic acid in vitro on HS 683, a glioma cell line, and to study the mechanism involved in the induction of cytotoxicity and apoptosis by TA. TA exhibited maximum cytotoxic activity against the Hs 683 cell line. Nuclear morphology, 4',6-diamidino-2-phenylindole staining and annexin V/propidium iodide apoptosis assaying of Hs 683 cells confirmed that cell death was due to the induction of apoptosis by TA. Further mechanistic study of TA on Hs 683 cells revealed that it decreased cell growth with increasing TA concentration, that resulted in the activation of pro-caspase 3 and caspase 9 and the cleavage of poly (ADP-ribose) polymerase, implying the induction of apoptosis cascades. Biochemical evidence of apoptosis resulted from the loss of mitochondrial membrane potential and increased intracellular reactive oxygen species production by TA in a dose-dependent manner. Based on this data, TA may be further investigated as a potential anticancer therapeutic lead.
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PMID:Tannic acid mediated induction of apoptosis in human glioma Hs 683 cells. 2984 85