NDLI: Vascular endothelial growth factor B coordinates metastasis of non-small cell lung cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liu, Gang Xu, Shengbao Jiao, Fanglei Ren, Tao Li, Qinchuan
Description	Country affiliation: China Author Affiliation: Liu G ( Department of Throatic Surgery, East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai, 200085, China.)
Abstract	Neovascularization is critical for the invasion and metastasis of non-small cell lung cancer (NSCLC). However, the molecular mechanism underlying the control of neovascularization of NSCLC is not completely understood. Both vascular endothelial growth factor B (VEGF-B) and matrix metalloproteinases 9 (MMP9) play essential roles in neovascularization of NSCLC. Here, we examined whether VEGF-B and MMP9 may affect each other to coordinate the neovascularization process in NSCLC. We found strong positive correlation of VEGF-B and MMP9 levels in the NSCLC from the patients. Moreover, patients that had NSCLC with metastasis had significantly higher levels of VEGF-B and MMP9 in the primary cancer. Using a human NSCLC line A549, we found that overexpression of VEGF-B increased expression of MMP9, while inhibition of VEGF-B decreased expression of MMP9. On the other hand, overexpression of MMP9 increased expression of VEGF-B, while inhibition of MMP9 decreased expression of VEGF-B. These data suggest that expression of VEGF-B and MMP9 may activate each other to enhance neovascularization. We then analyzed the underlying mechanism. Application of a specific ERK/MAPK inhibitor but not a PI3K/Akt inhibitor to VEGF-B-overexpressing A549 cells substantially abolished the effect of VEGF-B on MMP9 activation, while application of a specific PI3K/Akt inhibitor but not an ERK/MAPK inhibitor to MMP9-overexpressing A549 cells substantially abolished the effect of MMP9 on VEGF-B activation, suggesting that VEGF-B may activate MMP9 via ERK/MAPK signaling pathway, while MMP9 may activate VEGF-B via PI3K/Akt signaling pathway. Thus, our data highlight a coordinating relationship between VEGF-B and MMP9 in the regulation of neovascularization in NSCLC.
File Format	HTM / HTML
ISSN	10104283
Issue Number	3
Volume Number	36
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2015-03-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Carcinoma, Non-small-cell Lung Genetics Lung Neoplasms Vascular Endothelial Growth Factor B Cell Line, Tumor Cell Movement Humans Map Kinase Signaling System Matrix Metalloproteinase 9 Mitogen-activated Protein Kinases Neovascularization, Pathologic Phosphatidylinositol 3-kinases Proto-oncogene Proteins C-akt Signal Transduction Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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