Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.canlet.2011.09.040
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dc.titleTargeting p53 as a therapeutic strategy in sensitizing TRAIL-induced apoptosis in cancer cells
dc.contributor.authorZhao, J.
dc.contributor.authorLu, Y.
dc.contributor.authorShen, H.-M.
dc.date.accessioned2014-06-23T05:56:39Z
dc.date.available2014-06-23T05:56:39Z
dc.date.issued2012-01-01
dc.identifier.citationZhao, J., Lu, Y., Shen, H.-M. (2012-01-01). Targeting p53 as a therapeutic strategy in sensitizing TRAIL-induced apoptosis in cancer cells. Cancer Letters 314 (1) : 8-23. ScholarBank@NUS Repository. https://doi.org/10.1016/j.canlet.2011.09.040
dc.identifier.issn03043835
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/77562
dc.description.abstractTumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been intensively studied as a cancer therapeutic agent due to its unique ability to induce apoptosis in malignant cells but not in normal cells. However, as more human cancer cells are reported to be resistant to TRAIL treatment, it is important to develop new therapeutic strategies to overcome this resistance. p53 is an important tumor suppressor that is widely involved in cellular responses to various stresses. In this mini-review, we aim to provide an overview of the intricate relationship between p53 and the TRAIL-mediated apoptosis pathway, and to summarize the current approaches of targeting p53 as a therapeutic strategy to sensitize TRAIL-induced apoptosis in human cancer cells. Although in some cases TRAIL kills cancer cells in a p53-independent manner, it is believed that in cancers with wild-type and functional p53, targeting p53 may be an important strategy for overcoming TRAIL-resistance in cancer therapy. © 2011 Elsevier Ireland Ltd.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.canlet.2011.09.040
dc.sourceScopus
dc.subjectApoptosis
dc.subjectCancer
dc.subjectP53
dc.subjectSensitization
dc.subjectTRAIL
dc.typeOthers
dc.contributor.departmentCHEMISTRY
dc.contributor.departmentSAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
dc.description.doi10.1016/j.canlet.2011.09.040
dc.description.sourcetitleCancer Letters
dc.description.volume314
dc.description.issue1
dc.description.page8-23
dc.description.codenCALED
dc.identifier.isiut000298531900002
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