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Activation of p53-regulated pro-survival signals and hypoxia-independent mitochondrial targeting of TIGAR by human papillomavirus E6 oncoproteins
Virology. 2023 May 22;585:1-20. doi: 10.1016/j.virol.2023.05.004. Online ahead of print.ABSTRACTThe high-risk subtype human papillomaviruses (hrHPVs) infect and oncogenically transform basal epidermal stem cells associated with the development of squamous-cell epithelial cancers. The viral E6 oncoprotein destabilizes the p53 tumor suppressor, inhibits p53 K120-acetylation by the Tat-interacting protein of 60 kDa (TIP60, or Kat5), and prevents p53-dependent apoptosis. Intriguingly, the p53 gene is infrequently mutated in HPV + cervical cancer clinical isolates which suggests a possible paradoxical role for this gatekeeper i...
Source: Virology - May 31, 2023 Category: Virology Authors: Lacin Yapindi Tetiana Bowley Nick Kurtaneck Rachel L Bergeson Kylie James Jillian Wilbourne Carolyn K Harrod Brenda Y Hernandez Brooke M Emerling Courtney Yates Robert Harrod Source Type: research

Viruses, Vol. 7, Pages 5243-5256: HPV16 E6 Controls the Gap Junction Protein Cx43 in Cervical Tumour Cells
Human papillomavirus type 16 (HPV16) causes a range of cancers including cervical and head and neck cancers. HPV E6 oncoprotein binds the cell polarity regulator hDlg (human homologue of Drosophila Discs Large). Previously we showed in vitro, and now in vivo, that hDlg also binds Connexin 43 (Cx43), a major component of gap junctions that mediate intercellular transfer of small molecules. In HPV16-positive non-tumour cervical epithelial cells (W12G) Cx43 localised to the plasma membrane, while in W12T tumour cells derived from these, it relocated with hDlg into the cytoplasm. We now provide evidence that E6 regulates this ...
Source: Viruses - October 5, 2015 Category: Virology Authors: Peng SunLi DongAlasdair MacDonaldShahrzad AkbariMichael EdwardMalcolm HodginsScott JohnstoneSheila Graham Tags: Article Source Type: research

Inhibition of cervical cancer cell growth in vitro and in vivo by lentiviral-vector mediated shRNA targeting the common promoter of HPV16 E6 and E7 oncogenes.
Abstract Deregulated expression of high-risk human papillomavirus oncogenes (E6 and E7) is a pivotal event for pathogenesis and progression in cervical cancer. Both viral oncogenes are therefore regarded as ideal therapeutic targets. Small interfering RNAs (siRNA) or double-stranded RNAs can knock down target genes effectively through siRNA-induced transcriptional gene silencing (TGS). Here, we established lentiviral-vector mediated shRNA (LV-shRNA) targeting common promoter of HPV16 E6/E7 and targeting E6 transcript, transduced the lentiviral construct into cervical HPV16-positive cell lines Siha and Caski, then ...
Source: Antiviral Research - May 1, 2013 Category: Virology Authors: Zhou J, Li B, Peng C, Wang F, Fu Z, Zhou C, Hong D, Ye F, Lü W, Xie X Tags: Antiviral Res Source Type: research