Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the anti-cancer effect of a novel organoselenium compound BBSKE (1,2-[bis(1,2-Benzisoselenazolone-3(2H)-ketone)]ethane, BBSKE, PCT: CN02/00412) on cell growth and apoptosis, focusing on the protein activity of Thioredoxin Reductase (TrxR) and Caspase-3, in oral squamous cell carcinoma (OSCC) in vitro and in vivo. Oral squamous cancer cell line Tca8113 was treated with various concentrations of BBSKE. Growth and apoptosis as well as the protein activities were analyzed. Morphologic changes of Tca8113 cells after 24h treatment of BBSKE were determined by fluorescence microscopy. The increase of Caspase-3 activity and decrease of Thioredoxin reductase (TrxR) activity were also measured. BBSKE induced a significant cell growth inhibition and elicited typical apoptotic morphologic changes (chromatic condensation, nucleus fragmentation). This phenomenon was accompanied by a change in protein activity of Thioredoxin reductase (TrxR) and Caspase-3. The anti-cancer effect of BBSKE was then studied in well-established Tca8113 xenografts in nude mice. In those tumors, anti-cancer effects were observed and significantly higher than the controls. Together, these results indicate that BBSKE can inhibit tongue cancer cell proliferation in vitro and in vivo, and induce apoptosis in Tca8113 cell lines partially via inhibiting the activity of TrxR and promoting the activity of Caspase-3.
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PMID:The inhibitory effect of a novel organoselenium compound BBSKE on the tongue cancer Tca8113 in vitro and in vivo. 1828 84

The aim of this study was to characterize the role of CFTR during Cd(2+)-induced apoptosis. For this purpose primary cultures and cell lines originated from proximal tubules (PCT) of wild-type cftr(+/+) and cftr(-/-) mice were used. In cftr(+/+) cells, the application of Cd(2+) (5 microM) stimulated within 8 min an ERK1/2-activated CFTR-like Cl(-) conductance sensitive to CFTR(inh)-172. Thereafter Cd(2+) induced an apoptotic volume decrease (AVD) within 6 h followed by caspase-3 activation and apoptosis. The early increase in CFTR conductance was followed by the activation of volume-sensitive outwardly rectifying (VSOR) Cl(-) and TASK2 K(+) conductances. By contrast, cftr(-/-) cells exposed to Cd(2+) were unable to develop VSOR currents, caspase-3 activity, and AVD process and underwent necrosis. Moreover in cftr(+/+) cells, Cd(2+) enhanced reactive oxygen species (ROS) production and induced a 50% decrease in total glutathione content (major ROS scavenger in PCT). ROS generation and glutathione decrease depended on the presence of CFTR, since they did not occur in the presence of CFTR(inh)-172 or in cftr(-/-) cells. Additionally, Cd(2+) exposure accelerates effluxes of fluorescent glutathione S-conjugate in cftr(+/+) cells. Our data suggest that CFTR could modulate ROS levels to ensure apoptosis during Cd(2+) exposure by modulating the intracellular content of glutathione.
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PMID:CFTR mediates cadmium-induced apoptosis through modulation of ROS level in mouse proximal tubule cells. 1943 24