Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand

Human papillomavirus (HPV) E6 and E7 onco-proteins are essential factors for HPV oncogenesis. These E6 and E7 gene products play a central role in the induction of malignant transformation by interacting with several cellular regulatory proteins such as p16INK4a, p53 and nuclear factor κB (NF-κB). I...

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Main Authors: Senba M., Mori N., Fujita S., Jutavijittum P., Yousukh A., Toriyama K., Wada A.
Format: Article
Language:English
Published: 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-77954893556&partnerID=40&md5=ca594d6ead083a7a82456a3911a077d3
http://cmuir.cmu.ac.th/handle/6653943832/3653
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spelling th-cmuir.6653943832-36532014-08-30T02:35:10Z Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand Senba M. Mori N. Fujita S. Jutavijittum P. Yousukh A. Toriyama K. Wada A. Human papillomavirus (HPV) E6 and E7 onco-proteins are essential factors for HPV oncogenesis. These E6 and E7 gene products play a central role in the induction of malignant transformation by interacting with several cellular regulatory proteins such as p16INK4a, p53 and nuclear factor κB (NF-κB). In the present study, conducted in northern Thailand, HPV-DNA was detected in penile cancer cases using an in situ hybridization procedure and p16INK4a, p53 and NF-κB were detected by immunohistochemistry. Using the cell cycle regulatory proteins p16INK4a (61.5%) and p53 (71.8%), it was found that of the 51 cases, 39 (76.5%) were HPV-DNA-positive in penile cancer. On the other hand, 25% p16INK4a and 75% p53, respectively, were found in HPV-negative cases. Prevalence of HPV infection (76.5%) was shown in penile cancer cases in northern Thailand. No difference was found between HPV-positive and HPV-negative cases with respect to the presence of the cell cycle regulatory protein p53. On the other hand, p16INK4a was found to be different between HPV-positive and HPV-negative cases. Inactivation of tumor suppressor genes, such as p16INK4a and p53, to genetic instability, cell immortalization, accumulation of mutations and cancer formation, with or without HPV and irrespective of HPV infection, is therefore suggested. Of the 39 HPV-positive cases, 35 (89.7%) were NF-κB-positive in the nucleus, 29 (74.4%) in the cytoplasm and 37 (94.9%) in the nucleus and/or cytoplasm. NF-κB was detected in 4 (33.3%) of the 12 HPV-negative cases. Therefore, we propose that penile cancer cases with HPV infection are more likely to activate NF-κB than those without HPV infection. 2014-08-30T02:35:10Z 2014-08-30T02:35:10Z 2010 Article 17921074 10.3892/ol_00000106 http://www.scopus.com/inward/record.url?eid=2-s2.0-77954893556&partnerID=40&md5=ca594d6ead083a7a82456a3911a077d3 http://cmuir.cmu.ac.th/handle/6653943832/3653 English
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
language English
description Human papillomavirus (HPV) E6 and E7 onco-proteins are essential factors for HPV oncogenesis. These E6 and E7 gene products play a central role in the induction of malignant transformation by interacting with several cellular regulatory proteins such as p16INK4a, p53 and nuclear factor κB (NF-κB). In the present study, conducted in northern Thailand, HPV-DNA was detected in penile cancer cases using an in situ hybridization procedure and p16INK4a, p53 and NF-κB were detected by immunohistochemistry. Using the cell cycle regulatory proteins p16INK4a (61.5%) and p53 (71.8%), it was found that of the 51 cases, 39 (76.5%) were HPV-DNA-positive in penile cancer. On the other hand, 25% p16INK4a and 75% p53, respectively, were found in HPV-negative cases. Prevalence of HPV infection (76.5%) was shown in penile cancer cases in northern Thailand. No difference was found between HPV-positive and HPV-negative cases with respect to the presence of the cell cycle regulatory protein p53. On the other hand, p16INK4a was found to be different between HPV-positive and HPV-negative cases. Inactivation of tumor suppressor genes, such as p16INK4a and p53, to genetic instability, cell immortalization, accumulation of mutations and cancer formation, with or without HPV and irrespective of HPV infection, is therefore suggested. Of the 39 HPV-positive cases, 35 (89.7%) were NF-κB-positive in the nucleus, 29 (74.4%) in the cytoplasm and 37 (94.9%) in the nucleus and/or cytoplasm. NF-κB was detected in 4 (33.3%) of the 12 HPV-negative cases. Therefore, we propose that penile cancer cases with HPV infection are more likely to activate NF-κB than those without HPV infection.
format Article
author Senba M.
Mori N.
Fujita S.
Jutavijittum P.
Yousukh A.
Toriyama K.
Wada A.
spellingShingle Senba M.
Mori N.
Fujita S.
Jutavijittum P.
Yousukh A.
Toriyama K.
Wada A.
Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
author_facet Senba M.
Mori N.
Fujita S.
Jutavijittum P.
Yousukh A.
Toriyama K.
Wada A.
author_sort Senba M.
title Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
title_short Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
title_full Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
title_fullStr Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
title_full_unstemmed Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand
title_sort relationship among human papillomavirus infection, p16ink4a, p53 and nf-κb activation in penile cancer from northern thailand
publishDate 2014
url http://www.scopus.com/inward/record.url?eid=2-s2.0-77954893556&partnerID=40&md5=ca594d6ead083a7a82456a3911a077d3
http://cmuir.cmu.ac.th/handle/6653943832/3653
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