NDLI: N-myc downstream-regulated gene 1 promotes tumor inflammatory angiogenesis through JNK activation and autocrine loop of interleukin-1 by human gastric cancer cells.

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N-myc downstream-regulated gene 1 promotes tumor inflammatory angiogenesis through JNK activation and autocrine loop of interleukin-1 by human gastric cancer cells.

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N-myc downstream-regulated gene 1 promotes tumor inflammatory angiogenesis through JNK activation and autocrine loop of interleukin-1 by human gastric cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kuwano, Michihiko Ureshino, Hiroki Shibata, Tomohiro Watari, Kosuke Abe, Hideyuki Izumi, Hiroto Kawahara, Akihiko Mukaida, Naofumi Ono, Mayumi Uba, Manami Murakami, Yuichi
Description	Author Affiliation: Murakami Y ( Department of Pharmaceutical Oncology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.)
Abstract	The expression of N-myc downstream-regulated gene 1 (NDRG1) was significantly correlated with tumor angiogenesis and malignant progression together with poor prognosis in gastric cancer. However, the underlying mechanism for the role of NDRG1 in the malignant progression of gastric cancer remains unknown. Here we examined whether and how NDRG1 could modulate tumor angiogenesis by human gastric cancer cells. We established NU/Cap12 and NU/Cap32 cells overexpressing NDRG1 in NUGC-3 cells, which show lower tumor angiogenesis in vivo. Compared with parental NU/Mock3, NU/Cap12, and NU/Cap32 cells: 1) induced higher tumor angiogenesis than NU/Mock3 cells accompanied by infiltration of tumor-associated macrophages in mouse dorsal air sac assay and Matrigel plug assay; 2) showed much higher expression of CXC chemokines, MMP-1, and the potent angiogenic factor VEGF-A; 3) increased the expression of the representative inflammatory cytokine, IL-1 ; 4) augmented JNK phosphorylation and nuclear expression of activator protein 1 (AP-1). Further analysis demonstrated that knockdown of AP-1 (Jun and/or Fos) resulted in down-regulation of the expression of VEGF-A, CXC chemokines, and MMP-1, and also suppressed expression of IL-1 in NDRG1-overexpressing cell lines. Treatment with IL-1 receptor antagonist (IL-1ra) resulted in down-regulation of JNK and c-Jun phosphorylation, and the expression of VEGF-A, CXC chemokines, and MMP-1 in NU/Cap12 and NU/Cap32 cells. Finally, administration of IL-1ra suppressed both tumor angiogenesis and infiltration of macrophages by NU/Cap12 in vivo. Together, activation of JNK/AP-1 thus seems to promote tumor angiogenesis in relationship to NDRG1-induced inflammatory stimuli by gastric cancer cells.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	35
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-08-30
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Cycle Proteins Metabolism Interleukin-1alpha Intracellular Signaling Peptides And Proteins MAP Kinase Kinase 4 Neovascularization, Pathologic Stomach Neoplasms Animals Genetics Cell Line, Tumor Chemokines, CXC Enzyme Activation Gene Expression Regulation, Neoplastic Inflammation Pathology Interleukin-4 Macrophages Matrix Metalloproteinase 1 Matrix Metalloproteinase 13 Mice Mice, Inbred BALB C Neoplasms, Experimental Phosphorylation Transcription Factor AP-1 Vascular Endothelial Growth Factor A Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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