NDLI: IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma.

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IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dien Bard, Jennifer Gelebart, Pascal Anand, Mona Zak, Zoulika Hegazy, Samar A. Amin, Hesham M. Lai, Raymond
Description	Author Affiliation: Dien Bard J ( Department of Laboratory Medicine and Pathology, Cross Cancer Institute and University of Alberta, 11560 University Avenue, Edmonton, Alberta, Canada T6G 1Z2.)
Abstract	Interleukin (IL)-21 has been reported to both stimulate cell growth and promote survival in benign lymphoid cells and several types of hematopoietic neoplasms. It induces JAK3/STAT3 signaling, a biologically important cellular pathway activated in most cases of anaplastic lymphoma kinase (ALK)-expressing anaplastic large cell lymphoma (ALK(+)ALCL). Therefore, we hypothesize that IL-21 may contribute to JAK3/STAT3 activation and cell growth in ALK(+)ALCL. By reverse transcription-PCR, we found consistent expression of IL-21 receptor (IL-21R) in all ALK(+)ALCL cell lines and frozen tumors examined. IL-21 was also consistently expressed in ALK(+)ALCL tumors, although its mRNA was detectable in only one of three cell lines tested. By immunohistochemistry, we examined 10 paraffin-embedded ALK(+)ALCL tumors; all cases were positive for both IL-21 and IL-21R in these neoplastic cells. IL-21 signaling is biologically significant in ALK(+)ALCL since the addition of recombinant IL-21 enhanced the activation of JAK3/STAT3 and significantly increased cell growth in ALK(+)ALCL cell lines. However, small interfering RNA down-regulation of IL-21R significantly decreased both STAT3 activation and cell growth. IL-21R expression is not linked to nucleophosmin-ALK since forced expression of nucleophosmin-ALK and small interfering RNA down-regulation of nucleophosmin-ALK did not significantly change the expression of either IL-21R or IL-21. Our findings thus support the enhancement of JAK3/STAT3 activation and cell growth in ALK(+)ALCL via IL-21 signaling. These results further support the concept that constitutive activation of STAT3 in these tumors is multifactorial.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2009.080982
Journal	The American Journal of Pathology
Issue Number	2
Volume Number	175
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2009-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Receptors, Interleukin-21 Cell Proliferation Rna, Small Interfering Discipline Pathology Biosynthesis Pharmacology Metabolism Stat3 Transcription Factor Janus Kinase 3 Pathology Interleukins Receptor Protein-tyrosine Kinases Lymphoma, Large-cell, Anaplastic Cell Line, Tumor Protein-tyrosine Kinases Genetics Enzymology
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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