p73ß, unlike p53, suppresses growth and induces apoptosis of human papillomavirus E6-expressing cancer cells

Nitas Prabhu, Kumaravel Somasundaram, Kapaettu Satyamoorthy, Meenhard Herlyn, Wafik S. El-Deiry

    Research output: Contribution to journalArticle

    82 Citations (Scopus)

    Abstract

    Human papillomavirus (HPV) is the major cause of cervical cancer worldwide. HPV-E6 protein targets the p53 tumor suppressor protein for degradation by ubiquitin-mediated proteolysis making such cancers resistant to p53-gene therapy. Here we show that infection of human cancer cells by E6-expressing adenovirus (Ad-E6) leads to degradation of both wild-type or mutant p53 protein. Interestingly, the p53-homologue candidate tumor suppressor p73 is not degraded in Ad-E6 infected cancer cells. Wild-type p73ß and not wild-type p53 or mutant p73 is a potent inhibitor of cancer colony growth and inducer of apoptosis, despite HPV-E6 overexpression. The results suggest a novel strategy using p73ß in gene therapy of HPV-E6 expressing cancers.

    Original languageEnglish
    Pages (from-to)5-9
    Number of pages5
    JournalInternational Journal of Oncology
    Volume13
    Issue number1
    Publication statusPublished - 07-1998

    Fingerprint

    Apoptosis
    Growth
    Neoplasms
    Genetic Therapy
    Proteolysis
    Tumor Suppressor Protein p53
    p53 Genes
    Mutant Proteins
    Ubiquitin
    Adenoviridae
    Uterine Cervical Neoplasms
    Infection

    All Science Journal Classification (ASJC) codes

    • Oncology
    • Cancer Research

    Cite this

    Prabhu, Nitas ; Somasundaram, Kumaravel ; Satyamoorthy, Kapaettu ; Herlyn, Meenhard ; El-Deiry, Wafik S. / p73ß, unlike p53, suppresses growth and induces apoptosis of human papillomavirus E6-expressing cancer cells. In: International Journal of Oncology. 1998 ; Vol. 13, No. 1. pp. 5-9.
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    p73ß, unlike p53, suppresses growth and induces apoptosis of human papillomavirus E6-expressing cancer cells. / Prabhu, Nitas; Somasundaram, Kumaravel; Satyamoorthy, Kapaettu; Herlyn, Meenhard; El-Deiry, Wafik S.

    In: International Journal of Oncology, Vol. 13, No. 1, 07.1998, p. 5-9.

    Research output: Contribution to journalArticle

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    AB - Human papillomavirus (HPV) is the major cause of cervical cancer worldwide. HPV-E6 protein targets the p53 tumor suppressor protein for degradation by ubiquitin-mediated proteolysis making such cancers resistant to p53-gene therapy. Here we show that infection of human cancer cells by E6-expressing adenovirus (Ad-E6) leads to degradation of both wild-type or mutant p53 protein. Interestingly, the p53-homologue candidate tumor suppressor p73 is not degraded in Ad-E6 infected cancer cells. Wild-type p73ß and not wild-type p53 or mutant p73 is a potent inhibitor of cancer colony growth and inducer of apoptosis, despite HPV-E6 overexpression. The results suggest a novel strategy using p73ß in gene therapy of HPV-E6 expressing cancers.

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