Antiapoptotic proteins Bcl2 and BclX do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest
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| Natura: | Recurso digital |
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Zenodo
2006
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| _version_ | 1866902095465021440 |
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| author | GOMEZ CASARES, MARIA TERESA José P. Vaque Lemes Castellano, Agelina Molero Labarta, María Teresa Ferrandiz, Nuria Leon, Javier |
| author_facet | GOMEZ CASARES, MARIA TERESA José P. Vaque Lemes Castellano, Agelina Molero Labarta, María Teresa Ferrandiz, Nuria Leon, Javier |
| contents | <p>Imatinib (STI571), a Bcr-Abl kinase inhibitor, is widely used in chronic myeloid leukemia (CML). This study analyzes the effects of imatinib on proliferation and apoptosis in K562-derived CML cell lines with constitutive expression of the antiapoptotic genes Bcl2 and BclX. Imatinib-mediated apoptosis was completely abrogated in both Bcl2- and BclX-expressing cell lines; however, imatinib still inhibited proliferation, with growth arrest even stronger than in parental K562 cells. These results indicate that, besides its pro-apoptotic effect, imatinib can arrest cell growth through an apoptosis-independent mechanism.</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_18340076 |
| institution | Zenodo |
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| publishDate | 2006 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | Antiapoptotic proteins Bcl2 and BclX do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest GOMEZ CASARES, MARIA TERESA José P. Vaque Lemes Castellano, Agelina Molero Labarta, María Teresa Ferrandiz, Nuria Leon, Javier <p>Imatinib (STI571), a Bcr-Abl kinase inhibitor, is widely used in chronic myeloid leukemia (CML). This study analyzes the effects of imatinib on proliferation and apoptosis in K562-derived CML cell lines with constitutive expression of the antiapoptotic genes Bcl2 and BclX. Imatinib-mediated apoptosis was completely abrogated in both Bcl2- and BclX-expressing cell lines; however, imatinib still inhibited proliferation, with growth arrest even stronger than in parental K562 cells. These results indicate that, besides its pro-apoptotic effect, imatinib can arrest cell growth through an apoptosis-independent mechanism.</p> |
| title | Antiapoptotic proteins Bcl2 and BclX do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest |
| url | https://doi.org/10.5281/zenodo.18340076 |