Retention of cell adhesion and growth capability in human cervical cancer cells deprived of cell anchorage.
Cell adhesion is linked to various regulatory processes of growth as well as apoptotic cell death in normal and transformed epithelial cells. We investigated changes of cellular responses to the deprivation of cell anchorage associated with immortalization or malignant transformation. Normal human ectocervical keratinocytes (NCE cells) deprived of cell anchorage become susceptible to apoptosis, and in parallel they lose their adhesion to the culture substratum. The loss of cell adhesion is not directly due to apoptosis. NCE16 cells, an immortalized but not malignantly transformed subline of NCE, underwent apoptosis and lost cell adhesion in suspension, as the NCE cells did. By contrast, apoptosis was not inducible in human cervical cancer-derived C33A cells in suspension. Of other cell lines derived from human cervical cancer, SiHa cells showed a weak apoptotic response and Caski cells were highly sensitive to apoptosis in the absence of cell anchorage. Unlike NCE or NCE16 cells, all these cancer cells retained cell adhesion as well as growth capability in suspension cultures. These results indicate that retention of cell adhesion and growth capability in the absence of cell anchorage is more closely associated with cancer cell lines than resistance to apoptosis upon the deprivation of cell anchorage.
Kikuchi
K
K
Laboratory of Molecular Cell Biology, Kanagawa Cancer Center Research Institute, Yokohama. kkikuchi@yk.rim.or.jp
Yasumoto
S
S
D017209:Apoptosis; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects; D018929:Cell Culture Techniques; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002584:Cervix Uteri / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D003513:Cycloheximide / Q000494:pharmacology; D053938:DNA Fragmentation / Q000187:drug effects; D016521:Electrophoresis, Gel, Pulsed-Field; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007223:Infant; D007476:Ionophores / Q000494:pharmacology; D015603:Keratinocytes / Q000166:cytology / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D011480:Protease Inhibitors / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D002583:Uterine Cervical Neoplasms / Q000378:metabolism / Q000473:pathology*
D061945:Caspase Inhibitors; D007476:Ionophores; D011480:Protease Inhibitors; D011500:Protein Synthesis Inhibitors; C093260:benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene; D001224:Aspartic Acid; D000001:Calcimycin; D003513:Cycloheximide; D020169:Caspases; D002118:Calcium