| pubmed-article:8958222 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C1326205 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C0594374 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C2717970 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C0851287 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8958222 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:8958222 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:8958222 | pubmed:dateCreated | 1997-1-23 | lld:pubmed |
| pubmed-article:8958222 | pubmed:abstractText | Progress in the treatment of hepatocellular carcinoma (HCC), a common tumor worldwide, has been disappointing. Inhibitors of topoisomerases are being widely studied as potential inducers of tumor cell apoptosis. Our aims were to determine whether topoisomerase-directed drugs would induce apoptosis in a human HCC cell line (Hep 3B) and, if so, to investigate the mechanism. The topoisomerase I poison camptothecin (CPT) induced apoptosis of Hep 3B cells in a time- and concentration-dependent manner. In contrast, the topoisomerase II poison etoposide failed to induce apoptosis despite the apparent stabilization of topoisomerase II-DNA complexes. Unexpectedly, CPT-induced apoptosis in this cell type occurred without any detectable cleavage of poly(ADP-ribose) polymerase or lamin B, polypeptides that are commonly cleaved in other cell types undergoing apoptosis. Likewise, Hep 3B cell apoptosis occurred without a detectable increase in interleukin-1beta-converting enzyme (ICE)-like or cysteine protease P32 (CPP32)-like protease activity. In contrast, trypsin-like protease activity (cleavage of Boc-Val-Leu-Lys-chloromethylaminocoumarin in situ) increased threefold in cells treated with CPT but not etoposide. Tosyl-lysyl chloromethyl ketone inhibited the trypsin-like protease activity and diminished CPT-induced apoptosis. These data demonstrate that (a) apoptosis is induced in Hep 3B cells after stabilization of topoisomerase I-DNA complexes but not after stabilization of topoisomerase II-DNA complexes as measured by alkaline filter elution; (b) Hep 3B cell apoptosis occurs without activation of ICE-like and CPP32-like protease activity; and (c) a trypsin-like protease activity appears to contribute to apoptosis in this cell type. | lld:pubmed |
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| pubmed-article:8958222 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8958222 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8958222 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8958222 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8958222 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8958222 | pubmed:issn | 0021-9738 | lld:pubmed |
