Abstract
A reduced capacity for apoptosis induction is considered to play a significant role both in the development of malignancy and in tumor cell resistance to chemotherapeutic drugs. The Bcl-2 oncoprotein inhibits apoptosis induced by antitumor agents at a point downstream of drug-target interactions. Stable expression of Bcl-2 in the human epithelial tumor (HeLa) cell line results in inhibition of apoptosis following exposure to the topoisomerase II poison, etoposide. However, Bcl-2 is unable to enhance clonogenic survival as a result of alternate pathways to reproductive death induced by the drug. The purpose of this study was to further investigate the role of Bcl-2 in human epithelial tumor cell drug resistance using 5-fluoro-2'-deoxyuridine, staurosporine, and doxorubicin, in addition to etoposide. The ability of Bcl-2 to enhance clonogenic cell survival was studied by colony-forming assays, while delay of cell death induction was assessed by trypan blue viability measurements. The proportion of apoptotic cells was measured by morphological criteria, as well as detection of apoptotic DNA fragmentation using the terminal deoxynucleotidyl transferase assay. Despite profound inhibition to loss of plasma membrane integrity for all ...Continue Reading
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