An Antibody for Macrophage Migration Inhibitory Factor Suppresses Tumour Growth and Inhibits Tumour-Associated Angiogenesis

Ogawa, Hidehiko; Nishihira, Jun; Sato, Yuji; Kondo, Masao; Takahashi, Norihiko; Oshima, Takahiro; Todo, Satoru

doi:10.1006/cyto.1999.0562

Cited by 126 publications

(97 citation statements)

References 24 publications

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“…It has been suggested that MIF could promote colon cancer invasion and metastasis via the Rho-dependent pathway (40,41). Anti-MIF antibody has also been shown to suppress tumor growth in vivo and inhibits tumor-associated angiogenesis (42). S100A8 was another biomarker identified in the Apc Minϩ/Ϫ mouse adenomas, and we further confirmed that its expression increases as human CRC progresses from normal to higher stages (Duke's stages A-D) at both the protein and RNA levels in two relatively large human CRC sample sets.…”

Section: Discussionsupporting

confidence: 72%

Identification of Early Intestinal Neoplasia Protein Biomarkers Using Laser Capture Microdissection and MALDI MS

Xu¹,

Beauchamp

et al. 2009

Molecular & Cellular Proteomics

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Obtaining protein profiles from a homogeneous cell population in tissues can significantly improve our capability in protein biomarker discovery. In this study, unique protein profiles from the top and bottom sections of mouse crypts and Apc Min؉/؊ adenomas were obtained using laser capture microdissection (LCM) combined with MALDI MS. Statistically significant protein peaks with differential expression were selected, and a set of novel protein biomarkers were identified. Immunohistochemistry was performed to confirm the differentially expressed protein biomarkers found by LCM combined with MALDI MS. To validate the relevance of the findings in human colorectal cancer (CRC), S100A8 was further confirmed in human CRC using immunohistochemistry. In addition, S100A8 was found to have an increased expression at different human CRC stages (Duke's A-D) compared with controls at both protein (n ‫؍‬ 168 cases) and RNA (n ‫؍‬ 215 cases) levels. Overall LCM combined with MALDI MS is a promising method to identify intestinal protein biomarkers from minute amounts of tissue. The novel protein biomarkers identified from the top and bottom crypts will increase our knowledge of the specific protein changes taking place during cell migration from the crypt bottom to top. In addition, the identified cancer protein biomarkers will aid in the exploration of colorectal tumorigenesis mechanisms as well as in the advancement of molecularly based diagnosis of colorectal cancer. Molecular & Cellular Proteomics 8:936 -945, 2009.

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Section: Discussionsupporting

confidence: 72%

Identification of Early Intestinal Neoplasia Protein Biomarkers Using Laser Capture Microdissection and MALDI MS

Xu¹,

Beauchamp

et al. 2009

Molecular & Cellular Proteomics

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“…It has been reported that the vascularity of neuroblastoma in patients with widely metastatic disease is significantly higher than that in patients with local or regional disease, and that vascularity shows a strong inverse correlation with the survival of patients (Meitar et al, 1996). One of the important activities of MIF in promoting tumorigenesis and metastasis is to stimulate angiogenesis (Ogawa et al, 2000). Recent studies have shown that immunoneutralization of MIF during the initial stage of lymphoma growth has profound effects on tumor size (Chesney et al, 1999), and that MIF is a required factor for tumor-initiated endothelial cell proliferation (Yang et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of tumor growth and metastasis in vitro and in vivo by targeting macrophage migration inhibitory factor in human neuroblastoma

et al. 2006

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Macrophage migration inhibitory factor (MIF) has been defined as a novel oncogene. Our previous results have shown that MIF may contribute to the progression of neuroblastoma by (a) inducing N-Myc expression and (b) upregulating the expression of angiogenic factors. The aim of this study was to test whether tumor growth could be inhibited by reduction of endogenous MIF expression in neuroblastoma and clarify the molecular mechanisms underlying MIF reduction on the control of neuroblastoma growth. We established human neuroblastoma cell lines stably expressing antisense MIF (AS-MIF) cDNA. These stable transfectants were characterized by cell proliferation, gene expression profile, tumorigenicity and metastasis in vitro and in vivo. Decreased MIF expression was observed after transfection with AS-MIF in neuroblastoma cells and downregulation of MIF expression significantly correlated with decreased expression of NMyc, Ras, c-Met and TrkB at protein level. Affymetrix microarray analysis revealed that expression of IL-8 and c-met was inhibited and neuroblastoma-favorable genes such as EPHB6 and BLU were upregulated in MIF reduced cells. Neuroblastoma cell growth exhibited a nearly 80% reduction in AS-MIF transfectants in vitro. Furthermore, mice in which tumors formed after subcutaneous injection of AS-MIF transfectants showed a 90% reduction in tumor growth compared to control. Metastasis in mice was also suppressed dramatically. Our data demonstrate that targeting MIF expression is a promising therapeutic strategy in human neuroblastoma therapy, and also identifies the MIF target genes for further study.

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“…MIF is a cytokine that mediates host in¯ammatory and immune responses (for a review see Nishihira, 2000) and is up-regulated by transforming growth factor-b, PDGF, and FGF2 (Takahashi et al, 1998). Recently, immunoneutralization of MIF has been shown to inhibit tumor growth possibly by inhibiting endothelial cell proliferation (Ogawa et al, 2000). A170 was originally cloned as an oxidative stress-inducible gene (Ishii et al, 1996).…”

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confidence: 99%

Gene expression profile in fibroblast growth factor 2-transformed endothelial cells

et al. 2002

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Fibroblast growth factor-2 (FGF2) exerts paracrine and autocrine functions on endothelial cells. FGF2-overexpressing murine aortic endothelial cells (FGF2-T-MAE cells) induce opportunistic hemangioendothelioma-like tumors when inoculated in immunode®cient mice. To evaluate the impact of FGF2-mediated activation on gene expression pro®le in transformed endothelial cells, we performed subtractive suppression hybridization analysis between FGF2-T-MAE cells and parental MAE cells. The two cell populations were compared for di erential gene expression also by gene macroarray hybridization with 32 P-labeled cDNAs. The two approaches allowed the identi®cation of 27 transcripts whose expression was upregulated by FGF2 in endothelial cells. With the exception of one unknown gene, the di erentially expressed transcripts encoded for proteins involved in the modulation of cell cycle, di erentiation, and cell adhesion. Among them, the stress-inducible genes A170, GADD45 and GADD153 are upregulated by FGF2 transfection or recombinant growth factor treatment. Their expression was also induced in vascular tumors originated by parental or FGF2-transfected MAE cells in nude mice. This study extends the number of genes involved in tumor angiogenesis and/or endothelial cell transformation, a ®nding with possible implications for the discovery of novel targets for angiostatic therapy.

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An Antibody for Macrophage Migration Inhibitory Factor Suppresses Tumour Growth and Inhibits Tumour-Associated Angiogenesis

Cited by 126 publications

References 24 publications

Identification of Early Intestinal Neoplasia Protein Biomarkers Using Laser Capture Microdissection and MALDI MS

Identification of Early Intestinal Neoplasia Protein Biomarkers Using Laser Capture Microdissection and MALDI MS

Inhibition of tumor growth and metastasis in vitro and in vivo by targeting macrophage migration inhibitory factor in human neuroblastoma

Gene expression profile in fibroblast growth factor 2-transformed endothelial cells

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