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

详细信息    查看全文

• 作者：Gang Liu (1)
  Shengbao Xu (2)
  Fanglei Jiao (1)
  Tao Ren (2)
  Qinchuan Li (1)
  
  1. Department of Throatic Surgery ; East Hospital ; Tongji University School of Medicine ; 150 Jimo Road ; Shanghai ; 200085 ; China
  2. Lung Cancer Center ; East Hospital ; Tongji University School of Medicine ; Shanghai ; 200085 ; China
  
• 关键词：Vascular endothelial growth factor B (VEGF ; B) ; Matrix metalloproteinases 9 (MMP9) ; PI3K ; ERK/MAPK ; Non ; small cell lung cancer (NSCLC) ; Metastasis
• 刊名：Tumor Biology
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：36
• 期：3
• 页码：2185-2191
• 全文大小：314 KB
• 参考文献：1. Zarogoulidis, K, Zarogoulidis, P, Darwiche, K, Boutsikou, E, Machairiotis, N, Tsakiridis, K (2013) Treatment of non-small cell lung cancer (NSCLC). J Thorac Dis 5: pp. S389-96
  2. Mitsudomi, T, Suda, K, Yatabe, Y (2013) Surgery for NSCLC in the era of personalized medicine. Nat Rev Clin Oncol 10: pp. 235-44 CrossRef
  3. Pallis, AG, Syrigos, KN (2013) Epidermal growth factor receptor tyrosine kinase inhibitors in the treatment of NSCLC. Lung Cancer 80: pp. 120-30 CrossRef
  4. Jian, H, Zhao, Y, Liu, B, Lu, S (2014) SEMA4b inhibits MMP9 to prevent metastasis of non-small cell lung cancer. Tumour Biol.
  5. Pei, J, Lou, Y, Zhong, R, Han, B (2014) MMP9 activation triggered by epidermal growth factor induced foxo1 nuclear exclusion in non-small cell lung cancer. Tumour Biol 35: pp. 6673-8 CrossRef
  6. Wang, W, Wu, X, Tian, Y (2014) Crosstalk of AP4 and TGFbeta receptor signaling in NSCLC. Tumour Biol.
  7. Dufour, A, Overall, CM (2013) Missing the target: matrix metalloproteinase antitargets in inflammation and cancer. Trends Pharmacol Sci 34: pp. 233-42 CrossRef
  8. Ferrara, N (2009) Vascular endothelial growth factor. Arterioscler Thromb Vasc Biol 29: pp. 789-91 CrossRef
  9. Xiao, X, Prasadan, K, Guo, P, El-Gohary, Y, Fischbach, S, Wiersch, J (2014) Pancreatic duct cells as a source of VEGF in mice. Diabetologia 57: pp. 991-1000 CrossRef
  10. Xiao, X, Guo, P, Chen, Z, El-Gohary, Y, Wiersch, J, Gaffar, I (2013) Hypoglycemia reduces vascular endothelial growth factor a production by pancreatic beta cells as a regulator of beta cell mass. J Biol Chem 288: pp. 8636-46 CrossRef
  11. Cleaver, O, Melton, DA (2003) Endothelial signaling during development. Nat Med 9: pp. 661-8 CrossRef
  12. Ferrara, N, Gerber, HP, LeCouter, J (2003) The biology of VEGF and its receptors. Nat Med 9: pp. 669-76 CrossRef
  13. Carmeliet, P, Jain, RK (2011) Molecular mechanisms and clinical applications of angiogenesis. Nature 473: pp. 298-307 CrossRef
  14. Carrillo de Santa Pau, E, Arias, FC, Caso Pelaez, E, Munoz Molina, GM, Sanchez Hernandez, I, Muguruza Trueba, I (2009) Prognostic significance of the expression of vascular endothelial growth factors A, B, C, and D and their receptors R1, R2, and R3 in patients with nonsmall cell lung cancer. Cancer 115: pp. 1701-1712 CrossRef
  15. Riely, GJ, Miller, VA (2007) Vascular endothelial growth factor trap in non small cell lung cancer. Clin Cancer Res 13: pp. s4623-7 CrossRef
  16. Davidson, B, Reich, R, Risberg, B, Nesland, JM (2002) The biological role and regulation of matrix metalloproteinases (MMP) in cancer. Arkh Patol 64: pp. 47-53
  17. Rhee, JS, Coussens, LM (2002) Recking MMP function: implications for cancer development. Trends Cell Biol 12: pp. 209-11 CrossRef
  18. Zhou, X, Qi, Y (2014) Plgf inhibition impairs metastasis of larynx carcinoma through MMP3 downregulation. Tumour Biol 35: pp. 9381-6 CrossRef
  19. Wang, F, Xiao, W, Sun, J, Han, D, Zhu, Y (2014) Mirna-181c inhibits EGFR-signaling-dependent MMP9 activation via suppressing Akt phosphorylation in glioblastoma. Tumour Biol 35: pp. 8653-8 CrossRef
  20. Song, H, Tian, Z, Qin, Y, Yao, G, Fu, S, Geng, J (2014) Astrocyte elevated gene-1 activates MMP9 to increase invasiveness of colorectal cancer. Tumour Biol 35: pp. 6679-85 CrossRef
  21. Chen, Y, Jiang, T, Mao, A, Xu, J (2014) Esophageal cancer stem cells express PLGF to increase cancer invasion through MMP9 activation. Tumour Biol.
  22. Lieber, M, Smith, B, Szakal, A, Nelson-Rees, W, Todaro, G (1976) A continuous tumor-cell line from a human lung carcinoma with properties of type II alveolar epithelial cells. Int J Cancer 17: pp. 62-70 CrossRef
  23. Mao, D, Zhang, Y, Lu, H, Zhang, H (2014) Molecular basis underlying inhibition of metastasis of gastric cancer by anti-VEGFa treatment. Tumour Biol 35: pp. 8217-23 CrossRef
  
• 刊物主题：Cancer Research;
• 出版者：Springer Netherlands
• ISSN：1423-0380

文摘

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.