7 research outputs found
Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development
Persistent infection with high-risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, and host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response and only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions and CC. We present a review of recent research on the molecular mechanisms that allow HPV-infected cells to evade immune surveillance and potential targets of molecular therapy to inhibit tumor immune escape
Supplementary Material for: HPV 16 E2 Protein Induces Apoptosis in Human and Murine HPV 16 Transformed Epithelial Cells and Has Antitumoral Effects in vivo
<p><i>Objective:</i> Our aims were to examine the ability of the human
papillomaviruse (HPV) 16 E2 protein to induce apoptosis in a murine
HPV-transformed cell line, and to evaluate its antitumor properties on
HPV-associated tumors in vivo in immunocompetent mice. <i>Methods:</i>
HPV-transformed murine BMK-16/myc cells and human SiHa cells were
transfected with the HPV 16 E2 gene to examine the effects of the E2
protein on cell growth and on the E6 and E7 oncogenes as well as DNA
fragmentation and activation of the extrinsic pathway of apoptosis.
Finally, to test the antitumor effect of the E2 protein on an
experimental mouse tumor model, we generated a recombinant adenovirus
expressing the E2 protein. <i>Results:</i> The E2 protein inhibited the
growth of SiHa and BMK-16/myc cell lines, and repressed the E6 and E7
oncogenes. Moreover, the E2 protein induced DNA fragmentation and
apoptosis through activation of caspases 8 and 3 in BMK-16/myc cells. On
the other hand, E2 also showed antitumor effects in vivo. <i>Conclusions:</i>
Our findings indicate that E2 exerts pro-apoptotic activity in a murine
HPV-transformed cell line as well as an antitumor effect in vivo.</p