Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth.
p53-dependent apoptosis is a major determinant of its tumor suppressor activity and can be triggered by hypoxia. No p53 target is known to be induced by p53 or to mediate p53-dependent apoptosis during hypoxia. We report that p53 can directly upregulate expression of Bnip3L, a cell death inducer. Du...
| Main Authors: | , , , , , , , , , , |
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| פורמט: | Journal article |
| שפה: | English |
| יצא לאור: |
2004
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| _version_ | 1826278729096101888 |
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| author | Fei, P Wang, W Kim, S Wang, S Burns, T Sax, J Buzzai, M Dicker, D Mckenna, W Bernhard, E El-Deiry, W |
| author_facet | Fei, P Wang, W Kim, S Wang, S Burns, T Sax, J Buzzai, M Dicker, D Mckenna, W Bernhard, E El-Deiry, W |
| author_sort | Fei, P |
| collection | OXFORD |
| description | p53-dependent apoptosis is a major determinant of its tumor suppressor activity and can be triggered by hypoxia. No p53 target is known to be induced by p53 or to mediate p53-dependent apoptosis during hypoxia. We report that p53 can directly upregulate expression of Bnip3L, a cell death inducer. During hypoxia, Bnip3L is highly induced in wild-type p53-expressing cells, in part due to increased recruitment of p53 and CBP to Bnip3L. Apoptosis is reduced in hypoxia-exposed cells with functional p53 following Bnip3L knockdown. In vivo, Bnip3L knockdown promotes tumorigenicity of wild-type versus mutant p53-expressing tumors. Thus, Bnip3L, capable of attenuating tumorigenicity, mediates p53-dependent apoptosis under hypoxia, which provides a novel understanding of p53 in tumor suppression. |
| first_indexed | 2024-03-06T23:48:18Z |
| format | Journal article |
| id | oxford-uuid:71b9897b-f12f-4d42-b8c5-0f932ec72efd |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T23:48:18Z |
| publishDate | 2004 |
| record_format | dspace |
| spelling | oxford-uuid:71b9897b-f12f-4d42-b8c5-0f932ec72efd2022-03-26T19:45:25ZBnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:71b9897b-f12f-4d42-b8c5-0f932ec72efdEnglishSymplectic Elements at Oxford2004Fei, PWang, WKim, SWang, SBurns, TSax, JBuzzai, MDicker, DMckenna, WBernhard, EEl-Deiry, Wp53-dependent apoptosis is a major determinant of its tumor suppressor activity and can be triggered by hypoxia. No p53 target is known to be induced by p53 or to mediate p53-dependent apoptosis during hypoxia. We report that p53 can directly upregulate expression of Bnip3L, a cell death inducer. During hypoxia, Bnip3L is highly induced in wild-type p53-expressing cells, in part due to increased recruitment of p53 and CBP to Bnip3L. Apoptosis is reduced in hypoxia-exposed cells with functional p53 following Bnip3L knockdown. In vivo, Bnip3L knockdown promotes tumorigenicity of wild-type versus mutant p53-expressing tumors. Thus, Bnip3L, capable of attenuating tumorigenicity, mediates p53-dependent apoptosis under hypoxia, which provides a novel understanding of p53 in tumor suppression. |
| spellingShingle | Fei, P Wang, W Kim, S Wang, S Burns, T Sax, J Buzzai, M Dicker, D Mckenna, W Bernhard, E El-Deiry, W Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title | Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title_full | Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title_fullStr | Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title_full_unstemmed | Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title_short | Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. |
| title_sort | bnip3l is induced by p53 under hypoxia and its knockdown promotes tumor growth |
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