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• W2005536590 abstract "Cancer cells express different levels of apoptosis-promoting Bax protein. The present study evaluated whether induction of Bax initiates apoptosis and whether Bax overexpression enhances apoptosis induced by several chemotherapeutic agents in DLD-1 colon cancer cells, which originally express a high level of endogenous Bax protein and a low level of Bcl-2 protein. To investigate these two points, parental DLD-1 cells were transfected with the Tet-On Bax induction system (pTet-On and pTRE-Bax plasmids), and stable transduced cells were obtained. Induction of Bax by the Tet-On system initiated cytochrome c release from mitochondria, caspase-3 activation, and apoptosis to some extent in DLD-1 cells. Apoptosis induced by a chemotherapeutic agent, 5-fluorouracil, mitomycin C, paclitaxel, doxorubicin, or cisplatin, was enhanced by Bax overexpression. These findings suggest that Bax-overexpression-based gene therapy combined with chemotherapy would be effective in the treatment of colon cancer." @default.
• W2005536590 created "2016-06-24" @default.
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• W2005536590 date "2000-12-01" @default.
• W2005536590 modified "2023-10-13" @default.
• W2005536590 title "<i>Bax</i>Induction Activates Apoptotic Cascade via Mitochondrial Cytochrome<i>c</i>Release and<i>Bax</i>Overexpression Enhances Apoptosis Induced by Chemotherapeutic Agents in DLD-1 Colon Cancer Cells" @default.
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• W2005536590 doi "https://doi.org/10.1111/j.1349-7006.2000.tb00913.x" @default.
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