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Short Communications |
From the Cytokine/Cytokine Receptor Laboratory,*
LINK Laboratories, University of Massachusetts Cancer Center,
University of Massachusetts Medical School, Worcester; and the
Department of Pathology,
and the Division of
Hematology/ Oncology,
University of
Massachusetts/Memorial Health Care, Worcester, Massachusetts
Previous investigations have shown that interleukin-6, a
member of the JAK-STAT activating family of cytokines, plays an
important role in prostate carcinoma. Here we demonstrate the
co-expression of another member of this cytokine family,
interleukin-11 (IL-11), and components of its receptor
(interleukin-11 receptor; IL-11R), ie, IL-11R
(involved in ligand recognition), and gp130 (involved in signal
transduction) in cultured normal and malignant prostate-derived
epithelial cell lines. In the DU-145 prostate carcinoma cell
line, rhIL-11 stimulates a transient and dose-dependent
increase in the tyrosine 705-phosphorylated, active form of
STAT3 (STAT3 P-Tyr705), involved in the downstream signaling of
IL-11R and other members of the gp130-dependent receptors. The ability
of IL-11 to activate STAT3 in prostate-derived cells may be
mechanistically important, given recent data suggesting that
constitutively activated STAT3 may be associated with the malignant
phenotype. In 51 human primary tissues derived from normal
prostate, benign prostatic hyperplasia, and prostate
carcinomas, IL-11R and gp130 were commonly
expressed, with a statistically significant elevation in the
expression of IL-11R in prostate carcinoma. Also, the
tyrosine-phosphorylated, activated form of STAT3 was observed
more prominently in the nuclei of cells residing in malignant glands
compared to those in nonmalignant samples. Thus, the IL-11
receptor system is up-regulated in prostate carcinoma, and may
be one part of a cytokine network that maintains STAT3 in its activated
form in these tissues.
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