Compounds > 3-(4-dimethylamino-naphthalen-1-ylmethylene)-1-3-dihydro-indol-2-one

3-(4-dimethylamino-naphthalen-1-ylmethylene)-1-3-dihydro-indol-2-one and Stomach-Neoplasms

3-(4-dimethylamino-naphthalen-1-ylmethylene)-1-3-dihydro-indol-2-one has been researched along with Stomach-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for 3-(4-dimethylamino-naphthalen-1-ylmethylene)-1-3-dihydro-indol-2-one and Stomach-Neoplasms

Article	Year
Inhibition of Vascular Endothelial Growth Factor Receptor 3 Reduces Migration of Gastric Cancer Cells. Cancer investigation, 2015, Volume: 33, Issue:8 Angiogenesis induced by proangiogenic molecules such as vascular endothelial growth factor (VEGF) is a key process in the progression and metastasis of gastric cancer. In this study, we investigated the role of VEGF-C/VEGF receptor 3 (VEGFR3) axis in cell proliferation and migration/invasion of human gastric cancer cells (hGCCs). VEGF-C did not enhance cell proliferation but increased cell migration/invasion by approximately ∼50% in hGCCs (AGS and SNU-484). MAZ51, a VEGFR3 inhibitor, reduced the VEGF-C-induced increase in migration/invasion by ∼30% (p < 0.05). These results suggest that VEGFR3 could be a therapeutic target for reducing the metastasis of gastric cancer cells. Topics: Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; Indoles; Molecular Targeted Therapy; Naphthalenes; Protein Kinase Inhibitors; Stomach Neoplasms; Vascular Endothelial Growth Factor C; Vascular Endothelial Growth Factor Receptor-3	2015

Article

Year

Inhibition of Vascular Endothelial Growth Factor Receptor 3 Reduces Migration of Gastric Cancer Cells.

Cancer investigation, 2015, Volume: 33, Issue:8

Angiogenesis induced by proangiogenic molecules such as vascular endothelial growth factor (VEGF) is a key process in the progression and metastasis of gastric cancer. In this study, we investigated the role of VEGF-C/VEGF receptor 3 (VEGFR3) axis in cell proliferation and migration/invasion of human gastric cancer cells (hGCCs). VEGF-C did not enhance cell proliferation but increased cell migration/invasion by approximately ∼50% in hGCCs (AGS and SNU-484). MAZ51, a VEGFR3 inhibitor, reduced the VEGF-C-induced increase in migration/invasion by ∼30% (p < 0.05). These results suggest that VEGFR3 could be a therapeutic target for reducing the metastasis of gastric cancer cells.

Topics: Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; Indoles; Molecular Targeted Therapy; Naphthalenes; Protein Kinase Inhibitors; Stomach Neoplasms; Vascular Endothelial Growth Factor C; Vascular Endothelial Growth Factor Receptor-3

2015