RESUMEN
<p><b>OBJECTIVE</b>To investigate the expression feature of peroxiredoxin III in cervical lesions and to further understand the mechanism for cervical cancer development/progression.</p><p><b>METHODS</b>Expression of peroxiredoxin III was immunohistochemically detected in cervical cancer. In addition, cervical epithelia were transfected with recombinant adeno-associated virus vector containing human papillomavirus 16 E6/E7 and peroxiredoxin III expression was detected by quantitative real time PCR and Western blotting.</p><p><b>RESULTS</b>Peroxiredoxin III was significantly up-regulated in cervical cancer tissues. Nevertheless, expression of peroxiredoxin III remained unchanged in cervical epithelial cells after transfection.</p><p><b>CONCLUSION</b>It seems that Prx III is not related to cervical cancer initiation. Up-regulation of peroxiredoxin III in cervical cancer might be an active response to oxidative stress in malignant cells, which protects against oxidatiton-induced apoptosis.</p>
Asunto(s)
Femenino , Humanos , Persona de Mediana Edad , Cuello del Útero , Metabolismo , Regulación Neoplásica de la Expresión Génica , Papillomavirus Humano 16 , Genética , Metabolismo , Proteínas Oncogénicas Virales , Genética , Metabolismo , Proteínas E7 de Papillomavirus , Genética , Metabolismo , Peroxirredoxinas , Genética , Metabolismo , Proteínas Represoras , Genética , Metabolismo , Regulación hacia Arriba , Neoplasias del Cuello Uterino , Genética , Metabolismo , VirologíaRESUMEN
<p><b>BACKGROUND</b>To study the effect of human papillomavirus (HPV) 16 E6/E7 and TPA (12-O-tetradecanog-1-phorbol-13-acetate) on malignant transformation of human embryo oral tissue.</p><p><b>METHODS</b>Recombinant plasmid with HPV 16 E6/E7 was constructed and transfected into human embryo oral tissue. The oral tissue with HPV 16 E6/E7 gene or without the gene was inoculated into the hypophloeodal of right shoulder in scid mice, respectively. The study was conducted in four groups: the first group was the oral tissue transfected plasmid with HPV 16 E6/E7 plus TPA, which were inoculated into 8 scid mice; the second group was only oral tissue transfected with plasmid with HPV 16 E6/E7 into 6 scid mice; the third group was normal oral tissue plus TPA inoculated into 6 scid mice, and the final group was only normal oral tissue inoculated into 5 scid mice. Three days after inoculation, TPA was injected at the left shoulder of the mice once a week. Twelve weeks after inoculation, tumor was found in 7 scid mice from the first group. HPV 16 E6/E7 gene in tumor tissues was analyzed by PCR.</p><p><b>RESULTS</b>The rate of tumor formation was 7/8 in the first group; no tumor was found in the other groups. Pathological diagnosis of the tumor was fibrohistiocytoma. HPV 16 E6/E7 gene was detected by PCR in tumor tissues.</p><p><b>CONCLUSION</b>With the cooperating action of TPA, human oral tissue containing HPV 16 E6/E7 gene could cause malignant transformation in scid mice.</p>