Assessment of a capsid-modified E1B 55-kDa protein-deficient adenovirus vector for tumor treatment

Xun Ye, Qin Lu, Yi Zhao, Zhen Ren, Xia Meng, Sheng Fang Ge, Qi Hong Qiu, Yong Tong, Andre Lieber, Min Liang, Fang Hu, Hong Zhuan Chen

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


ONYX-015 and H101 are E1B 55-kDa protein-deficient replicating C group adenoviruses that are currently in clinical trials as antitumor agents. However, their application in cancer gene therapy is limited by the native tropism of C group adenoviruses. This is in part due to low expression of the C group adenovirus receptor (coxsackievirus-adenovirus receptor, CAR) on malignant tumors. An H101-based chimeric virus vector containing sequences encoding the Ad35 fiber domain instead of the Ad5 fiber (H101-F35) was constructed. This modification allowed infection of tumor cells through CD46, a membrane protein over-expressed on tumors. The CAR and CD46 RNA expression was evaluated by RT-PCR method. H101-F35 conferred a stronger cytocidal effect than H101 and ONYX-015 in tumor cell lines that lacked CAR expression (MDA-MB-435 and MCF-7), while the cytocidal effect of H101-35, H101 and ONYX-015 was similar in high-level CAR expressing cancer cell lines (A549, NCI-H446, Hep3B, LNCaP, ZR-75-30 and Bcap-37). In an MDA-MB-435 xenograft mouse tumor model, tumor growth in mice receiving H101-F35 was significantly inhibited compared with mice injected with H101. These results suggest that the chimeric oncolytic adenovirus H101-F35 vector might be a useful candidate for gene therapy of cancer.

Original languageEnglish
Pages (from-to)1156-1164
Number of pages9
JournalProgress in Biochemistry and Biophysics
Issue number12
StatePublished - Dec 2005


  • Adenovirus
  • Oncolytic
  • Transductional control


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