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Macrophage inhibitory factor 1 acts as a potential biomarker in patients with esophageal squamous cell carcinoma and is a target for antibody-based therapy.

Wang XB, Jiang XR, Yu XY, Wang L, He S, Feng FY, Guo LP, Jiang W, Lu SH - Cancer Sci. (2014)

Bottom Line: The results showed that the serum MIC1 of ESCC was significantly higher than normal groups (P < 0.001), and was positively associated with tumor invasion (P = 0.030) as well as lymph node metastasis (P = 0.007).The antibody of MIC1 inhibited the tumor growth (P < 0.001), and showing preference for tumor tissues in xenograft model.The decreased formation of neovascularization lumen may be involved in the mechanism.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

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The tumor tissue necrosis and inhibition of angiogenesis in vivo. (a) Representative hematoxylin and eosin-stained tumor tissues obtained from mice in the control (i, iv), 2 mg/kg treated group (ii, v) and 10 mg/kg treated group (iii, vi). (b) Detection of blood vessels via immunohistochemical staining for Von Willebrand factor (VWF) from the control group (i), 2 mg/kg treated group (ii), 10 mg/kg treated group (iii). (c) Quantification of angiogenesis assessed by microvessel density (MVD). Data represent the mean ± standard error (SE), n = 4. (d) The effect of macrophage inhibitory factor (MIC) and anti-MIC1 antibody on human umbilical vein endothelial cells (HUVECs) in vitro; Data represent the mean ± SE, n = 4.
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fig05: The tumor tissue necrosis and inhibition of angiogenesis in vivo. (a) Representative hematoxylin and eosin-stained tumor tissues obtained from mice in the control (i, iv), 2 mg/kg treated group (ii, v) and 10 mg/kg treated group (iii, vi). (b) Detection of blood vessels via immunohistochemical staining for Von Willebrand factor (VWF) from the control group (i), 2 mg/kg treated group (ii), 10 mg/kg treated group (iii). (c) Quantification of angiogenesis assessed by microvessel density (MVD). Data represent the mean ± standard error (SE), n = 4. (d) The effect of macrophage inhibitory factor (MIC) and anti-MIC1 antibody on human umbilical vein endothelial cells (HUVECs) in vitro; Data represent the mean ± SE, n = 4.

Mentions: In vitro study of cell proliferation showed that anti-MIC1 antibody did not significantly inhibit MIC1 overexpression cell line S4 (Fig. S2c). To investigate the mechanism of tumor inhibition by anti-MIC1 antibody, we conducted a simple analysis on xenograft tissues. Histopathological examination of the H&E staining slides showed that there was obvious tumor cell necrosis observed in anti-hMIC1 monoclonal antibody group (Fig. 5a). Von Willebrand factor IHC staining of Paraffin sections showed that MVD of neovascularization in the experimental group were significantly less than that of the control group (P < 0.001; Fig. 5b,c). In vitro study further confirmed that MIC1 can stimulate cell proliferation of HUVECs (P < 0.001; Fig. 5d) and the effect can be inhibited with anti-MIC1 antibody. These results suggest that neutralization of MIC1 reduces tumor angiogenesis in vivo.


Macrophage inhibitory factor 1 acts as a potential biomarker in patients with esophageal squamous cell carcinoma and is a target for antibody-based therapy.

Wang XB, Jiang XR, Yu XY, Wang L, He S, Feng FY, Guo LP, Jiang W, Lu SH - Cancer Sci. (2014)

The tumor tissue necrosis and inhibition of angiogenesis in vivo. (a) Representative hematoxylin and eosin-stained tumor tissues obtained from mice in the control (i, iv), 2 mg/kg treated group (ii, v) and 10 mg/kg treated group (iii, vi). (b) Detection of blood vessels via immunohistochemical staining for Von Willebrand factor (VWF) from the control group (i), 2 mg/kg treated group (ii), 10 mg/kg treated group (iii). (c) Quantification of angiogenesis assessed by microvessel density (MVD). Data represent the mean ± standard error (SE), n = 4. (d) The effect of macrophage inhibitory factor (MIC) and anti-MIC1 antibody on human umbilical vein endothelial cells (HUVECs) in vitro; Data represent the mean ± SE, n = 4.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317821&req=5

fig05: The tumor tissue necrosis and inhibition of angiogenesis in vivo. (a) Representative hematoxylin and eosin-stained tumor tissues obtained from mice in the control (i, iv), 2 mg/kg treated group (ii, v) and 10 mg/kg treated group (iii, vi). (b) Detection of blood vessels via immunohistochemical staining for Von Willebrand factor (VWF) from the control group (i), 2 mg/kg treated group (ii), 10 mg/kg treated group (iii). (c) Quantification of angiogenesis assessed by microvessel density (MVD). Data represent the mean ± standard error (SE), n = 4. (d) The effect of macrophage inhibitory factor (MIC) and anti-MIC1 antibody on human umbilical vein endothelial cells (HUVECs) in vitro; Data represent the mean ± SE, n = 4.
Mentions: In vitro study of cell proliferation showed that anti-MIC1 antibody did not significantly inhibit MIC1 overexpression cell line S4 (Fig. S2c). To investigate the mechanism of tumor inhibition by anti-MIC1 antibody, we conducted a simple analysis on xenograft tissues. Histopathological examination of the H&E staining slides showed that there was obvious tumor cell necrosis observed in anti-hMIC1 monoclonal antibody group (Fig. 5a). Von Willebrand factor IHC staining of Paraffin sections showed that MVD of neovascularization in the experimental group were significantly less than that of the control group (P < 0.001; Fig. 5b,c). In vitro study further confirmed that MIC1 can stimulate cell proliferation of HUVECs (P < 0.001; Fig. 5d) and the effect can be inhibited with anti-MIC1 antibody. These results suggest that neutralization of MIC1 reduces tumor angiogenesis in vivo.

Bottom Line: The results showed that the serum MIC1 of ESCC was significantly higher than normal groups (P < 0.001), and was positively associated with tumor invasion (P = 0.030) as well as lymph node metastasis (P = 0.007).The antibody of MIC1 inhibited the tumor growth (P < 0.001), and showing preference for tumor tissues in xenograft model.The decreased formation of neovascularization lumen may be involved in the mechanism.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Show MeSH
Related in: MedlinePlus