Glioblastoma Factors Increase the Migration of Human Brain Endothelial Cells In Vitro by Increasing MMP-9/CXCR4 Levels

被引:13
作者
De Oliveira Rosario, Luciane Vieira [1 ]
Da Rosa, Barbara Gomes [2 ]
Goncalves, Thaynan Lopes [1 ]
Lourenco Matias, Diana Isabel [3 ]
Freitas, Catarina [2 ]
Ferrer, Valeria Pereira [4 ]
机构
[1] Paulo Niemeyer State Brain Inst, Brains Biomed Lab, Rio De Janeiro, Brazil
[2] Univ Fed Rio de Janeiro, Biomed Sci Inst, Cellular Morphogenesis Lab, Rio De Janeiro, Brazil
[3] UCL, Dept Chem, Battaglias Lab, Christopher Ingold Bldg, London, England
[4] Fluminense Fed Univ, Inst Biol, Dept Cellular & Mol Biol, 30 Mario Santos Braga St, Niteroi, RJ, Brazil
关键词
Angiogenesis; endothelial cells; glioblastoma; cell crosstalk; MMP-9; CXCR4; GROWTH-FACTOR RECEPTOR-2; TUMOR ANGIOGENESIS; MESSENGER-RNA; UP-REGULATION; TENASCIN-C; CROSS-TALK; VEGF; EXPRESSION; PROLIFERATION; INVASION;
D O I
10.21873/anticanres.14244
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background/Aim: Glioblastoma (GB) is the most aggressive type of tumor in the central nervous system and is characterized by resistance to therapy and abundant vasculature. Tumor vessels contribute to the growth of GB, and the tumor microenvironment is thought to influence tumor vessels. We evaluated the molecular communication between human GB cells and human brain microvascular endothelial cells (HBMEC) in vitro. Materials and Methods: We investigated whether GB-conditioned media (GB-CM) influenced HBMEC proliferation and migration, as well as the levels of MMP-9, CXCL12, CXCR4, CXCR7, VEGFs, VEGFR-2, and WNT5a in HBMEC. Results: Although HBMEC proliferation was not modified, increased HBMEC migration was detected after GB-CM treatment. Furthermore, treatment of HBMEC with GB-CM resulted in increased levels of MMP-9 and CXCR4. The levels of WNT5a, VEGFs and VEGFR-2 were not affected. Conclusion: GB-secreted factors lead to increased endothelial cell migration and to increased levels of MMP-9 and CXCR4.
引用
收藏
页码:2725 / 2737
页数:13
相关论文
共 85 条
[1]   Structure and function of the blood-brain barrier [J].
Abbott, N. Joan ;
Patabendige, Adjanie A. K. ;
Dolman, Diana E. M. ;
Yusof, Siti R. ;
Begley, David J. .
NEUROBIOLOGY OF DISEASE, 2010, 37 (01) :13-25
[2]   Alternatively spliced vascular endothelial growth factor receptor-2 is an essential endogenous inhibitor of lymphatic vessel growth [J].
Albuquerque, Romulo J. C. ;
Hayashi, Takahiko ;
Cho, Won Gil ;
Kleinman, Mark E. ;
Dridi, Sami ;
Takeda, Atsunobu ;
Baffi, Judit Z. ;
Yamada, Kiyoshi ;
Kaneko, Hiroki ;
Green, Martha G. ;
Chappell, Joe ;
Wilting, Joerg ;
Weich, Herbert A. ;
Yamagami, Satoru ;
Amano, Shiro ;
Mizuki, Nobuhisa ;
Alexander, Jonathan S. ;
Peterson, Martha L. ;
Brekken, Rolf A. ;
Hirashima, Masanori ;
Capoor, Seema ;
Usui, Tomohiko ;
Ambati, Balamurali K. ;
Ambati, Jayakrishna .
NATURE MEDICINE, 2009, 15 (09) :1023-U74
[3]   VASCULAR ENDOTHELIAL GROWTH-FACTOR ACTS AS A SURVIVAL FACTOR FOR NEWLY FORMED RETINAL-VESSELS AND HAS IMPLICATIONS FOR RETINOPATHY OF PREMATURITY [J].
ALON, T ;
HEMO, I ;
ITIN, A ;
PEER, J ;
STONE, J ;
KESHET, E .
NATURE MEDICINE, 1995, 1 (10) :1024-1028
[4]   Tenascin-C in the extracellular matrix promotes the selection of highly proliferative and tubulogenesis-defective endothelial cells [J].
Alves, Tercia Rodrigues ;
da Fonseca, Anna Carolina Carvalho ;
Nunes, Sara Santana ;
da Silva, Aline Oliveira ;
Feijo Dubois, Luiz Gustavo ;
Faria, Jane ;
Kahn, Suzana Assad ;
Viana, Nathan Bessa ;
Marcondes, Jorge ;
Legrand, Chantal ;
Moura-Neto, Vivaldo ;
Morandi, Veronica .
EXPERIMENTAL CELL RESEARCH, 2011, 317 (15) :2073-2085
[5]   Propranolol adrenergic blockade inhibits human brain endothelial cells tubulogenesis and matrix metalloproteinase-9 secretion [J].
Annabi, Borhane ;
Lachambre, Marie-Paule ;
Plouffe, Karine ;
Moumdjian, Robert ;
Beliveau, Richard .
PHARMACOLOGICAL RESEARCH, 2009, 60 (05) :438-445
[6]   Cellular and molecular mechanisms of glioblastoma malignancy: Implications in resistance and therapeutic strategies [J].
Balca-Silva, Joana ;
Matias, Diana ;
do Carmo, Analia ;
Sarmento-Ribeiro, Ana Bela ;
Lopes, Maria Celeste ;
Moura-Neto, Vivaldo .
SEMINARS IN CANCER BIOLOGY, 2019, 58 :130-141
[7]   Glioblastoma entities express subtle differences in molecular composition and response to treatment [J].
Balca-Silva, Joana ;
Matias, Diana ;
Do Carmo, Analia ;
Dubois, Luiz Gustavo ;
Goncalves, Ana Cristina ;
Girao, Henrique ;
Silva Canedo, Nathalie Henriques ;
Coreia, Ana Helena ;
De Souza, Jorge Marcondes ;
Sarmento-Ribeiro, Ana Bela ;
Lopes, Maria Celeste ;
Moura-Neto, Vivaldo .
ONCOLOGY REPORTS, 2017, 38 (03) :1341-1352
[8]   A feed-forward loop between nuclear translocation of CXCR4 and HIF-1α promotes renal cell carcinoma metastasis [J].
Bao, Yi ;
Wang, Zhixiang ;
Liu, Bing ;
Lu, Xin ;
Xiong, Ying ;
Shi, Jiazi ;
Li, Peng ;
Chen, Junming ;
Zhang, Zongqin ;
Chen, Ming ;
Wang, Linhui ;
Wu, Zhenjie .
ONCOGENE, 2019, 38 (06) :881-895
[9]   Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling [J].
Benedito, Rui ;
Rocha, Susana F. ;
Woeste, Marina ;
Zamykal, Martin ;
Radtke, Freddy ;
Casanovas, Oriol ;
Duarte, Antonio ;
Pytowski, Bronislaw ;
Adams, Ralf H. .
NATURE, 2012, 484 (7392) :110-+
[10]  
Benjamin Mina M, 2012, Exp Suppl, V103, P209, DOI 10.1007/978-3-0348-0364-9_7