Interleukin-4 induced proliferation in normal human keratinocytes is associated with c-myc gene expression and inhibited by genistein

Cited 33 time in scopus
Metadata Downloads
Title
Interleukin-4 induced proliferation in normal human keratinocytes is associated with c-myc gene expression and inhibited by genistein
Author(s)
Young Yang; Hyun Mi Yoo; In Pyo Choi; Kwang Ho Pyun; Si Myung Byun; Hyunjung Ha
Bibliographic Citation
Journal of Investigative Dermatology, vol. 107, no. 3, pp. 367-372
Publication Year
1996
Abstract
We studied the effect of IL-4 on the proliferation of cultured normal human keratinocytes. Keratinocyte proliferation was stimulated by IL-4 and inhibited by anti-IL-4 antibody in a concentration-dependent manner. Anti-IL-6 antibody did not inhibit normal human keratinocyte proliferation, suggesting that the IL-4 could directly induce proliferation of these cells. IL-4 significantly induced cell cycle G0/G1 to S phase progression. The keratinocyte proliferation by IL-4 was mediated through one of the growth control genes, c-myc protooncogene. The expression of c-myc mRNA was significantly increased after IL-4 treatment of the keratinocytes, suggesting that c-myc plays a key role in the control of proliferation. The signal transduction pathways induced by IL-4 in the keratinocytes were studied with inhibitors of signal transduction. Genistein, a tyrosine kinase inhibitor, suppressed the level of the induced c-myc mRNA expression, but H7, a serine/threonine kinase inhibitor, and okadaic acid, a protein phosphatase 1 and 2A inhibitor, did not block the induced c-myc gene expression. Taken together, these results suggest that IL-4 stimulates the proliferation of keratinocytes in vitro by promoting a transition from G0/G1 to S phase of the cell cycle. Induction of c-myc after IL-4 treatment could indicate an important role for c-myc in the proliferation of keratinocytes. Our observations also suggest that tyrosine kinases may be involved in IL-4-induced proliferation.
Keyword
cell cycletyrosine kinase
ISSN
0022-202X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1111/1523-1747.ep12363346
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.