JAK pathway induction of c-Myc critical to IL-5 stimulation of cell proliferation and inhibition of apoptosis

Wei Hwa Lee, Fu Hwa Liu, John Yi Chung Lin, Shih Yun Huang, Heng Lin, Wei Ju Liao, Huei Mei Huang

研究成果: 雜誌貢獻文章

7 引文 (Scopus)

摘要

Interleukin-5 (IL-5) induction of c-Myc expression is associated with IL-5 inhibition of apoptosis in hematopoietic cells. In this study, TFa1 and TFa8 cells with stable overexpression of IL-5 receptor α (IL-5Rα) subunit in TF-1 cells, a human hematopoietic progenitor cell line which expressed low levels of IL-5Rα, were used to explored how IL-5 up-regulate c-Myc and the role of c-Myc in IL-5 signaling. First, we demonstrate that IL-5 induced c-Myc RNA and protein expressions, as well as activated Janus kinases (JAK1 and JAK2) and signal transducer and activator of transcription-5b (STAT5b). JAK inhibitor AG490 and c-Myc inhibitor 10058-F4, both, reduced IL-5-mediated cell proliferation in a dose- and time-dependent manner. Both, AG490 and 10058-F4, also reduced IL-5-mediated anti-apoptotic activity. Furthermore, AG490 inhibited IL-5-mediated c-Myc induction and promoter activity. We further examined the role of JAK1 and JAK2 in the induction of c-Myc expression using the CDJAK fusion proteins, which consisted of a CD16 extracellular domain, a CD7 transmembrane domain, and either JAK1 (CDJAK1) or JAK2 (CDJAK2) as intracellular domains. Simultaneous activation of JAK1 and JAK2 by anti-CD16 antibody crosslinking of CDJAK1 and CDJAK2 could induced c-Myc expression and promoter activity; AG490 inhibited CDJAK1 and CDJAK2-mediated effects. These results suggest that IL-5 induces cell proliferation and anti-apoptosis through the JAK/c-Myc pathway, and that JAK1 and JAK2 activation participate in IL-5-induced up-regulation of c-Myc. J. Cell. Biochem. 106: 929-936, 2009.

原文英語
頁(從 - 到)929-936
頁數8
期刊Journal of Cellular Biochemistry
106
發行號5
DOIs
出版狀態已發佈 - 四月 1 2009
對外發佈Yes

指紋

Interleukin-5
Cell proliferation
Cell Proliferation
Apoptosis
Interleukin-5 Receptors
Up-Regulation
Chemical activation
STAT5 Transcription Factor
Proto-Oncogene Proteins c-myc
Janus Kinases
Hematopoietic Stem Cells
Crosslinking
Anti-Idiotypic Antibodies
Proteins
Fusion reactions
Cells
RNA
Cell Line
alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide
Antibodies

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

引用此文

JAK pathway induction of c-Myc critical to IL-5 stimulation of cell proliferation and inhibition of apoptosis. / Lee, Wei Hwa; Liu, Fu Hwa; Lin, John Yi Chung; Huang, Shih Yun; Lin, Heng; Liao, Wei Ju; Huang, Huei Mei.

於: Journal of Cellular Biochemistry, 卷 106, 編號 5, 01.04.2009, p. 929-936.

研究成果: 雜誌貢獻文章

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abstract = "Interleukin-5 (IL-5) induction of c-Myc expression is associated with IL-5 inhibition of apoptosis in hematopoietic cells. In this study, TFa1 and TFa8 cells with stable overexpression of IL-5 receptor α (IL-5Rα) subunit in TF-1 cells, a human hematopoietic progenitor cell line which expressed low levels of IL-5Rα, were used to explored how IL-5 up-regulate c-Myc and the role of c-Myc in IL-5 signaling. First, we demonstrate that IL-5 induced c-Myc RNA and protein expressions, as well as activated Janus kinases (JAK1 and JAK2) and signal transducer and activator of transcription-5b (STAT5b). JAK inhibitor AG490 and c-Myc inhibitor 10058-F4, both, reduced IL-5-mediated cell proliferation in a dose- and time-dependent manner. Both, AG490 and 10058-F4, also reduced IL-5-mediated anti-apoptotic activity. Furthermore, AG490 inhibited IL-5-mediated c-Myc induction and promoter activity. We further examined the role of JAK1 and JAK2 in the induction of c-Myc expression using the CDJAK fusion proteins, which consisted of a CD16 extracellular domain, a CD7 transmembrane domain, and either JAK1 (CDJAK1) or JAK2 (CDJAK2) as intracellular domains. Simultaneous activation of JAK1 and JAK2 by anti-CD16 antibody crosslinking of CDJAK1 and CDJAK2 could induced c-Myc expression and promoter activity; AG490 inhibited CDJAK1 and CDJAK2-mediated effects. These results suggest that IL-5 induces cell proliferation and anti-apoptosis through the JAK/c-Myc pathway, and that JAK1 and JAK2 activation participate in IL-5-induced up-regulation of c-Myc. J. Cell. Biochem. 106: 929-936, 2009.",
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T1 - JAK pathway induction of c-Myc critical to IL-5 stimulation of cell proliferation and inhibition of apoptosis

AU - Lee, Wei Hwa

AU - Liu, Fu Hwa

AU - Lin, John Yi Chung

AU - Huang, Shih Yun

AU - Lin, Heng

AU - Liao, Wei Ju

AU - Huang, Huei Mei

PY - 2009/4/1

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N2 - Interleukin-5 (IL-5) induction of c-Myc expression is associated with IL-5 inhibition of apoptosis in hematopoietic cells. In this study, TFa1 and TFa8 cells with stable overexpression of IL-5 receptor α (IL-5Rα) subunit in TF-1 cells, a human hematopoietic progenitor cell line which expressed low levels of IL-5Rα, were used to explored how IL-5 up-regulate c-Myc and the role of c-Myc in IL-5 signaling. First, we demonstrate that IL-5 induced c-Myc RNA and protein expressions, as well as activated Janus kinases (JAK1 and JAK2) and signal transducer and activator of transcription-5b (STAT5b). JAK inhibitor AG490 and c-Myc inhibitor 10058-F4, both, reduced IL-5-mediated cell proliferation in a dose- and time-dependent manner. Both, AG490 and 10058-F4, also reduced IL-5-mediated anti-apoptotic activity. Furthermore, AG490 inhibited IL-5-mediated c-Myc induction and promoter activity. We further examined the role of JAK1 and JAK2 in the induction of c-Myc expression using the CDJAK fusion proteins, which consisted of a CD16 extracellular domain, a CD7 transmembrane domain, and either JAK1 (CDJAK1) or JAK2 (CDJAK2) as intracellular domains. Simultaneous activation of JAK1 and JAK2 by anti-CD16 antibody crosslinking of CDJAK1 and CDJAK2 could induced c-Myc expression and promoter activity; AG490 inhibited CDJAK1 and CDJAK2-mediated effects. These results suggest that IL-5 induces cell proliferation and anti-apoptosis through the JAK/c-Myc pathway, and that JAK1 and JAK2 activation participate in IL-5-induced up-regulation of c-Myc. J. Cell. Biochem. 106: 929-936, 2009.

AB - Interleukin-5 (IL-5) induction of c-Myc expression is associated with IL-5 inhibition of apoptosis in hematopoietic cells. In this study, TFa1 and TFa8 cells with stable overexpression of IL-5 receptor α (IL-5Rα) subunit in TF-1 cells, a human hematopoietic progenitor cell line which expressed low levels of IL-5Rα, were used to explored how IL-5 up-regulate c-Myc and the role of c-Myc in IL-5 signaling. First, we demonstrate that IL-5 induced c-Myc RNA and protein expressions, as well as activated Janus kinases (JAK1 and JAK2) and signal transducer and activator of transcription-5b (STAT5b). JAK inhibitor AG490 and c-Myc inhibitor 10058-F4, both, reduced IL-5-mediated cell proliferation in a dose- and time-dependent manner. Both, AG490 and 10058-F4, also reduced IL-5-mediated anti-apoptotic activity. Furthermore, AG490 inhibited IL-5-mediated c-Myc induction and promoter activity. We further examined the role of JAK1 and JAK2 in the induction of c-Myc expression using the CDJAK fusion proteins, which consisted of a CD16 extracellular domain, a CD7 transmembrane domain, and either JAK1 (CDJAK1) or JAK2 (CDJAK2) as intracellular domains. Simultaneous activation of JAK1 and JAK2 by anti-CD16 antibody crosslinking of CDJAK1 and CDJAK2 could induced c-Myc expression and promoter activity; AG490 inhibited CDJAK1 and CDJAK2-mediated effects. These results suggest that IL-5 induces cell proliferation and anti-apoptosis through the JAK/c-Myc pathway, and that JAK1 and JAK2 activation participate in IL-5-induced up-regulation of c-Myc. J. Cell. Biochem. 106: 929-936, 2009.

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KW - C-Myc

KW - Cell proliferation

KW - IL-5

KW - JAK

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