Abstract:
:The p53 tumor suppressor pathway is impaired in more than 90% of cervical cancers and cancer-derived cell lines as a result of infection by human papillomavirus (HPV). The HPV E6 oncoprotein forms complexes with p53 and promotes its degradation via ubiquitin-dependent mechanism. In our study, we attempted to improve the clinical outcomes of this combined therapy by modifying the p53-targeted adenovirus to become radiation-responsive. The antitumor adenovirus was constructed by inserting a radiation-responsive expression cassette composed of the promoter of early growth response-1 (Egr-1) and the proapoptotic protein TRAIL. We showed that the addition of adenovirus containing Egr-1/TRAIL significantly increased cell death and apoptosis caused by radiotherapy. In mice bearing xenograft tumors, intratumoral administration of the Egr-1/TRAIL adenovirus followed by radiation significantly reduced tumor growth and enhanced tumor survival. Our Egr-1/TRAIL adenoviral gene product may offer a novel "one-two punch" tumor therapy for cervical cancers not only by potentiating radiation treatment but also by preserving p53 defect-specific tumor killing of the oncolytic adenovirus.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Wang H,Song X,Zhang H,Zhang J,Shen X,Zhou Y,Fan X,Dai L,Qian G,Hoffman AR,Hu JF,Ge Sdoi
10.1002/ijc.26013subject
Has Abstractpub_date
2012-01-15 00:00:00pages
443-53issue
2eissn
0020-7136issn
1097-0215journal_volume
130pub_type
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journal_title:International journal of cancer
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