Adenovirus-mediated transfer of the p53 family genes, p73 and p51/p63 induces cell cycle arrest and apoptosis in colorectal cancer cell ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-09-01

AUTHORS

Y Sasaki, I Morimoto, S Ishida, T Yamashita, K Imai, T Tokino

ABSTRACT

p53 gene therapy is being tested clinically for the treatment of human cancer, however, some cancer models (in vivo and in vitro) are resistant to p53. To explore the potential use of two p53 homologues, p73 and p51/p63, in cancer gene therapy, we introduced p53, p73 and p51/p63 into colorectal cancer cell lines via adenoviral vectors, and compared their effects on cell growth. Among 10 cell lines tested, six cell lines displayed a similar response following transduction of p53, p73β or p51A/p63γ; two lines underwent cell-cycle arrest, three lines exhibited apoptosis and one line showed no-effect following transduction. The effect on cell-cycle progression was variable in the other four cell lines. Interestingly, three cell lines were resistant to p53-mediated apoptosis, including two lines having endogenous wild-type p53 alleles, but underwent apoptosis after transduction of p73β or p51A/p63γ. Similar to p53, transduction of p51A/p63γ induced extensive apoptosis when combined with adriamycin or X-radiation in SW480 cells, which are normally resistant to apoptosis. Transduction of p73β and p51A/p63γ also reduced the tumorigenicity of two colorectal cancer cells in vivo. These results suggest that adenovirus-mediated p73β and p51A/p63γ transfer are potential novel approaches for the treatment of human cancers, particularly for tumors that are resistant to p53 gene therapy. Gene Therapy (2001) 8, 1401–1408. More... »

PAGES

1401-1408

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.gt.3301538

DOI

http://dx.doi.org/10.1038/sj.gt.3301538

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11571580


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43 schema:description Abstractp53 gene therapy is being tested clinically for the treatment of human cancer, however, some cancer models (in vivo and in vitro) are resistant to p53. To explore the potential use of two p53 homologues, p73 and p51/p63, in cancer gene therapy, we introduced p53, p73 and p51/p63 into colorectal cancer cell lines via adenoviral vectors, and compared their effects on cell growth. Among 10 cell lines tested, six cell lines displayed a similar response following transduction of p53, p73β or p51A/p63γ; two lines underwent cell-cycle arrest, three lines exhibited apoptosis and one line showed no-effect following transduction. The effect on cell-cycle progression was variable in the other four cell lines. Interestingly, three cell lines were resistant to p53-mediated apoptosis, including two lines having endogenous wild-type p53 alleles, but underwent apoptosis after transduction of p73β or p51A/p63γ. Similar to p53, transduction of p51A/p63γ induced extensive apoptosis when combined with adriamycin or X-radiation in SW480 cells, which are normally resistant to apoptosis. Transduction of p73β and p51A/p63γ also reduced the tumorigenicity of two colorectal cancer cells in vivo. These results suggest that adenovirus-mediated p73β and p51A/p63γ transfer are potential novel approaches for the treatment of human cancers, particularly for tumors that are resistant to p53 gene therapy. Gene Therapy (2001) 8, 1401–1408.
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53 alleles
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57 arrest
58 cancer
59 cancer cell lines
60 cancer cells
61 cancer gene therapy
62 cancer model
63 cell cycle arrest
64 cell cycle progression
65 cell growth
66 cell lines
67 cells
68 colorectal cancer
69 colorectal cancer cell lines
70 colorectal cancer cells
71 cycle arrest
72 effect
73 extensive apoptosis
74 family genes
75 gene therapy
76 genes
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84 p51/p63
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105 tumorigenicity
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