Bullatacin, a potent antitumor annonaceous acetogenin, inhibits proliferation of human hepatocarcinoma cell line 2.2.15 by apoptosis induction.
ABSTRACT Bullatacin, isolated from the fruit of Annona atemoya, is one of the most potentially effective antitumor annonaceous acetogenins. Bullatacin was studied here for its ability to inhibit the proliferation of 2.2.15 cells, hepatitis B virus (HBV) DNA transfected human hepatocarcinoma cell line. It was found that bullatacin induced cytotoxicity of 2.2.15 cells in a time- and dose-dependent manner. Fifty percent effective dose (ED50) on day 1 of exposure to bullatacin were 7.8 +/- 2.5 nM for 2.2.15 cells. [3H]-Thymidine incorporation assays showed almost the same results. Bullatacin-treatment also reduced concentrations of hepatitis B surface antigen (HBsAg) in the cultured medium released from 2.2.15 cells, coincident with the decrease in the cell proliferation. Analysis of mophological changes of bullatacin-treated 2.2.15 by inverted phase-contrast microscope and eletron microscopy revealed a possible model of action for bullatacin to inhibit proliferation of 2.2.15 cells by inducing apoptosis. Most of the bullatacin-induced cell death was found to be due to apoptosis, as determined by double staining with fluorescein-isothiocyanate (FITC)-labeled annexin V and propidium iodide (PI).
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ABSTRACT: Cancer cells catabolise nutrients in a different way than healthy cells. Healthy cells mainly rely on oxidative phosphorylation, while cancer cells employ aerobic glycolysis. Glucose is the main nutrient catabolised by healthy cells, while cancer cells often depend on catabolism of both glucose and glutamine. A key organelle involved in this altered metabolism is mitochondria. Mitochondria coordinate the catabolism of glucose and glutamine across the cancer cell. Targeting mitochondrial metabolism in cancer cells has potential for the treatment of this disease. Perhaps the most promising target is the hexokinase-voltage dependent anion channel-adenine nucleotide translocase complex that spans the outer- and inner-mitochondrial membranes. This complex links glycolysis, oxidative phosphorylation and mitochondrial-mediated apoptosis in cancer cells. This review discusses cancer cell mitochondrial metabolism and the small molecule inhibitors of this metabolism that are in pre-clinical or clinical development.Pharmaceutical Research 09/2011; 28(11):2731-44. · 4.74 Impact Factor
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ABSTRACT: Cancer is one of the leading causes of death in humans. It is believed that plants can provide potential bioactive compounds for the development of "new leads" to combat cancer and other diseases. The present study focuses on the ability of the different extracts (aqueous, methanol, and chloroform) of the leaves of Zea mays in influencing the process of apoptosis induced by hydrogen peroxide (H2O2) in Hep2 (laryngeal carcinoma) cells. Various apoptosis-related parameters, such as cell viability, morphological changes, nuclear changes, and apoptotic index were characterized. sulforhodamine B and MTT assays were used to quantify the extent of cell death in the group exposed to H2O2, plant extracts, and their combination. Treatment with H2O2 caused cytotoxicity in cancer cells. The administration of leaf extract also caused an increase in the death of cancer cells. Oxidatively stressed cancer cells co-treated with all the Z. mays leaf extracts (except the chloroform extract) demonstrated cytotoxicity on a par with the H2O2-treated groups. This indicated that the aqueous and methanol leaf extracts did not influence the cytotoxic action of H2O2 in the cancer cells. Thus, various apoptosis-related events in Hep2 cells exposed to leaf extract throw light on the potential anticancer activity of the Z. mays leaves. The maximum activity was exerted by the methanolic extract followed by the aqueous and chloroform extracts.Journal of acupuncture and meridian studies. 06/2013; 6(3):149-158.
- Journal of Acupuncture and Meridian Studies 06/2013; 6(3).