Cancer Research Meeting Calendar  Telomeres
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

Cancer Research 67, 7765, August 15, 2007. doi: 10.1158/0008-5472.CAN-07-0014
© 2007 American Association for Cancer Research

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Reiterer, G.
Right arrow Articles by Yen, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reiterer, G.
Right arrow Articles by Yen, A.

Cell, Tumor, and Stem Cell Biology

Platelet-Derived Growth Factor Receptor Regulates Myeloid and Monocytic Differentiation of HL-60 Cells

Gudrun Reiterer and Andrew Yen

Department of Biomedical Sciences, Cornell University, Ithaca, New York

Requests for reprints: Andrew Yen, Department of Biomedical Sciences, T4-008 VRT, Cornell University, Ithaca, NY 14853. Phone: 607-253-3354; Fax: 607-253-3317; E-mail: ay13{at}cornell.edu.

Here, we show that the platelet-derived growth factor receptor (PDGFR) regulates myeloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid (RA) and vitamin D3 (D3), respectively. Both RA and D3 decreased the expression of PDGFR-{alpha} and PDGFR-ß throughout differentiation. When cells were treated with the PDGFR inhibitor AG1296 in addition to RA or D3, signs of terminal differentiation such as inducible oxidative metabolism and cell substrate adhesion were enhanced. These changes were accompanied by an increased extracellular signal-regulated kinase 1/2 activation. AG1296 also resulted in elevated expression of differentiation markers CD11b and CD66c when administered with RA or D3. Interestingly, other markers did not follow the same pattern. Cells receiving AG1296 in addition to RA or D3 showed decreased G1-G0 arrest and CD14, CD38, and CD89 expression. We thus provide evidence that certain sets of differentiation markers can be enhanced, whereas others can be inhibited by the PDGFR pathway. In addition, we found calcium levels to be decreased by RA and D3 but increased when AG1296 was given in addition to RA or D3, suggesting that calcium levels decrease during myeloid or monocytic differentiation, and elevated calcium levels can disturb the expression of certain differentiation markers. [Cancer Res 2007;67(16):7765–71]




This article has been cited by other articles:


Home page
J. Leukoc. Biol.Home page
S. J. A. M. Santegoets, A. J. M. van den Eertwegh, A. A. van de Loosdrecht, R. J. Scheper, and T. D. de Gruijl
Human dendritic cell line models for DC differentiation and clinical DC vaccination studies
J. Leukoc. Biol., December 1, 2008; 84(6): 1364 - 1373.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
M. Shen and A. Yen
c-Cbl Interacts with CD38 and Promotes Retinoic Acid-Induced Differentiation and G0 Arrest of Human Myeloblastic Leukemia Cells
Cancer Res., November 1, 2008; 68(21): 8761 - 8769.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. Wang and A. Yen
A MAPK-positive Feedback Mechanism for BLR1 Signaling Propels Retinoic Acid-triggered Differentiation and Cell Cycle Arrest
J. Biol. Chem., February 15, 2008; 283(7): 4375 - 4386.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2007 by the American Association for Cancer Research.