help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brody, J. R.
Right arrow Articles by Pasternack, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brody, J. R.
Right arrow Articles by Pasternack, G. R.
(American Journal of Pathology. 2004;164:273-283.)
© 2004 American Society for Investigative Pathology

pp32 Reduction Induces Differentiation of TSU-Pr1 Cells

Jonathan R. Brody, Shrihari S. Kadkol, M. Claire Hauer, Fatemeh Rajaii, Jessica Lee and Gary R. Pasternack

From the Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland

pp32 (ANP32A) is a nuclear phosphoprotein expressed as a nonmutated form in self-renewing cell populations and neoplastic cells. Mechanistically, pp32 may regulate pathways important in the process of differentiation as part of separate complexes inhibiting histone acetylation and regulating immediate-early and cytokine mRNA stability. Prostatic adenocarcinomas express pp32 in a differentiation related manner—well-differentiated tumors express lower levels of pp32 than poorly differentiated tumors. In benign prostate, pp32 is expressed in basal cells but not in terminally differentiated glandular cells. Based on these observations, we hypothesized that reduction of pp32 expression might be an important differentiation signal. We used anti-sense pp32 and RNAi transfection to study the effects of reduced pp32 expression in the TSU-Pr1 carcinoma cell line. pp32 reduction induced TSU-Pr1 cells to differentiate into neuronal-like cells with associated inhibition of growth. Reduction of pp32 and consequent differentiation were accompanied by a marked reduction in expression of SET, which complexes with pp32, by a marked change in acetylation status of histone H4, and by further differential expression of genes in differentiation pathways. Thus, reduction of pp32 in the undifferentiated TSU-Pr1 neoplastic cell line induces differentiation and thus may be an element of a differentiation control pathway in both normal and neoplastic cells.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
O. Adegbola and G. R. Pasternack
Phosphorylated Retinoblastoma Protein Complexes with pp32 and Inhibits pp32-mediated Apoptosis
J. Biol. Chem., April 22, 2005; 280(16): 15497 - 15502.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. N. Kutney, R. Hong, T. Macfarlan, and D. Chakravarti
A Signaling Role of Histone-binding Proteins and INHAT Subunits pp32 and Set/TAF-I{beta} in Integrating Chromatin Hypoacetylation and Transcriptional Repression
J. Biol. Chem., July 16, 2004; 279(29): 30850 - 30855.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Society for Investigative Pathology.