Home Neoplasma 2011 Neoplasma Vol.58, No.6, p.525-531, 2011

Journal info

6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.58, No.6, p.525-531, 2011

Title: Leukemic cells modulate induction of COX-2 in human stromal fibroblasts

Abstract: The interaction of cancer cells with surrounding normal tissue cells is of utmost importance for their survival and tumor progression. For these purposes the cancer cells exploit normal tissue responses associated with inflammation and tissue repair. In the immediate tumor microenvironment one of the early stromal markers is cyclooxygenase-2 (COX-2).
In this study we evaluated the effect of leukemia cell lines on nemosis-induced COX-2 expression in stromal fibroblasts. We found that THP-1 cells were the most potent leukemic cells (IC50=746) to suppress COX-2 expression. The U-937 cell line exhibited similar suppressive potency (IC50=921), whereas the KG-1 cell line (IC50=3519) was the least potent to affect COX-2 expression in the stromal cells.
Our study shows that human leukemic cells can actively participate in modulation of stromal inflammation via inhibition of COX-2 expression. In a co-culture model of leukemia cell lines and stromal fibroblasts, our data suggest that the tumor-stromal interactions are complexly regulated, and the straightforward association of COX-2 expression with tumor progression may require re-evaluation since some tumor cells, e.g. from hematologic malignancies, may differentially modulate inflammation and COX-2 expression.

Keywords: human leukemia cells, inflammation, COX-2, nemosis
Year: 2011, Volume: 58, Issue: 6 Page From: 525, Page To: 531
Price: 16.80 €

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.