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| Item Type: | Article |
|---|---|
| Title: | Equivalent effect of DNA damage-induced apoptotic cell death or long-term cell cycle arrest on colon carcinoma cell proliferation and tumour growth |
| Creators Name: | Bhonde, M.R. and Hanski, M.L. and Notter, M. and Gillissen, B.F. and Daniel, P.T. and Zeitz, M. and Hanski, C. |
| Abstract: | Knowledge of the type of biological reaction to chemotherapy is a prerequisite for its rational enhancement. We previously showed that irinotecan-induced DNA damage triggers in the HCT116p53wt colon carcinoma cell line a long-term cell cycle arrest and in HCT116p53-/- cells apoptosis (Magrini et al., 2002). To compare the contribution of long-term cell cycle arrest and that of apoptosis to inhibition of cell proliferation after irinotecan-induced DNA damage, we used this isogenic system as well as the cell lines LS174T (p53wt) and HT-29 (p53mut). Both p53wt cell lines responded to damage by undergoing a long-term tetraploid G1 arrest, whereas the p53mut cell lines underwent apoptosis. Cell cycle arrest as well as apoptosis caused a similar delay in cell proliferation. Irinotecan treatment also induced in mouse tumours derived from the p53wt cell lines a tetraploid G1 arrest and in those derived from the p53-deficient cell lines a transient G2/M arrest and apoptosis. The delay of tumour growth was in the same range in both groups, that is, arrest- and apoptosis-mediated tumour growth inhibition was comparable. In conclusion, cell cycle arrest as well as apoptosis may be equipotent mechanisms mediating the chemotherapeutic effects of irinotecan. |
| Keywords: | apoptosis, cell cycle arrest, chemotherapy, colon carcinoma, irinotecan |
| Source: | Oncogene |
| ISSN: | 0950-9232 |
| Publisher: | Nature Publishing Group |
| Volume: | 25 |
| Page Range: | 165-175 |
| Date: | 12 January 2006 |
| Official Publication: | https://doi.org/10.1038/sj.onc.1209017 |
| PubMed: | View item in PubMed |
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