Abstract:
:Virtually all cervical cancer morbidities are associated with genital skin or mucosa cell infection with human papillomavirus (HPV). The HPV oncogenic proteins E6 and E7 are able to inactivate p53 and Rb proteins, which results in malignant transformation. Employing quantitative real-time PCR and Western blot analysis, we observed that apicidin histone deacetylase (HDAC) inhibitor significantly reduced HPV16-E6 and -E7 transcripts and protein levels in SiHa cervical cancer cells. Moreover, we found that apicidin lowered HPV16-E6 and -E7 transcript stability and significantly decreased these transcripts' half-life from approximately 5h to 2h and from 6h to 3h, respectively. Our results from experiments with protein biosynthesis inhibitor suggest the involvement of an RNase and/or mRNA stabilization protein in HPV16-E6 and -E7 transcript stabilization. Since the HPV type 16 is associated with most cervical cancer incidence and HDAC inhibitors are being tested in anti-cancer clinical trials, our observations may have clinical significance.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Luczak MW,Jagodzinski PPdoi
10.1016/j.canlet.2008.06.030subject
Has Abstractpub_date
2008-12-08 00:00:00pages
53-60issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(08)00527-2journal_volume
272pub_type
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