| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Animal: DNA Viruses |
North Shore – Long Island Jewish Research Institute and Department of Otolaryngology and Communicative Disorders, Long Island Jewish Medical Center, 270-05 76th Avenue, New Hyde Park, New York 11040, USA1
Author for correspondence: Bettie Steinberg. Fax +1 718 347 2320. e-mail bsteinbe{at}lij.edu
Laryngeal papillomas are caused by infection of the laryngeal epithelium by human papillomavirus type 6 or type 11 (HPV-6/-11). Previous studies in our laboratory have demonstrated an increase in PI3 kinase levels in papilloma tissue. However, activation of the downstream effector of PI3 kinase, protein kinase B (PKB/Akt), was reduced. This observation was explained by the elevated expression of the phosphatase and tensin homologue (PTEN), a recently characterized tumour suppressor, in papilloma tissue. Recent investigation of the possible functional roles of PTEN during papilloma development has now indicated that the level of tyrosine(705)-phosphorylated signal transducer and activator of transcription 3 [PTyr(705)STAT3] could be inversely correlated to that of PTEN as well. In vitro phosphatase assays suggested the presence of an increased level of a PTyr(705)STAT3 phosphatase in papilloma extract. Immunodepletion of PTEN from papilloma extracts resulted in a reduction of the PTyr(705)STAT3 phosphatase activity. Transfection of PTEN cDNA into HeLa cells attenuated STAT3 phosphorylation at Tyr(705) in a dose-dependent manner. This attenuation of STAT3 phosphorylation was independent of the STAT3 kinase. Interestingly, introduction of a lipid phosphatase mutant of PTEN (G129E) resulted in heightened PTyr(705)STAT3 phosphatase activity, relative to that obtained from wild-type PTEN transfection. These data indicate that PTEN negatively regulates STAT3 activation in HPV-infected papilloma cells. Induction of PTEN and reduction of activated STAT3 might be a result of a host defence mechanism or a virus-directed strategy to alter normal epithelial differentiation programming.
This article has been cited by other articles:
|
|
 |
|
  K. S. Ahn, G. Sethi, B. Sung, A. Goel, R. Ralhan, and B. B. Aggarwal Guggulsterone, a Farnesoid X Receptor Antagonist, Inhibits Constitutive and Inducible STAT3 Activation through Induction of a Protein Tyrosine Phosphatase SHP-1 Cancer Res., June 1, 2008; 68(11): 4406 - 4415. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. K. Pathak, M. Bhutani, A. S. Nair, K. S. Ahn, A. Chakraborty, H. Kadara, S. Guha, G. Sethi, and B. B. Aggarwal Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells Mol. Cancer Res., September 1, 2007; 5(9): 943 - 955. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Bhutani, A. K. Pathak, A. S. Nair, A. B. Kunnumakkara, S. Guha, G. Sethi, and B. B. Aggarwal Capsaicin Is a Novel Blocker of Constitutive and Interleukin-6-Inducible STAT3 Activation Clin. Cancer Res., May 15, 2007; 13(10): 3024 - 3032. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Wu, A. L. Abramson, M. J. Shikowitz, A. J. Dannenberg, and B. M. Steinberg Epidermal Growth Factor-Induced Cyclooxygenase-2 Expression Is Mediated through Phosphatidylinositol-3 Kinase, Not Mitogen-Activated Protein/Extracellular Signal-Regulated Kinase Kinase, in Recurrent Respiratory Papillomas Clin. Cancer Res., September 1, 2005; 11(17): 6155 - 6161. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. J. Patel, A. Hansen, A. L. Merati, and J. E. Kerschner STAT3 Activation in Recurrent Respiratory Papillomatosis Arch Otolaryngol Head Neck Surg, September 1, 2004; 130(9): 1043 - 1045. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | MICROBIOLOGY | J GEN VIROL |
| J MED MICROBIOL | ALL SGM JOURNALS | |
