scholarly journals Live-Cell Imaging Assays to Study Glioblastoma Brain Tumor Stem Cell Migration and Invasion

10.3791/58152 ◽  
2018 ◽  
Author(s):  
Ian Restall ◽  
Danielle Anne Bozek ◽  
Charles Chesnelong ◽  
Samuel Weiss ◽  
H. Artee Luchman
Keyword(s):  
Stem Cell ◽  
Cell Migration ◽  
Brain Tumor ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Tumor Stem Cell ◽  
Migration And Invasion ◽  
Brain Tumor Stem Cell ◽  
Cell Migration And Invasion ◽  
Stem Cell Migration

scholarly journals The Study of Brain Tumor Stem Cell Migration

2018 ◽  
pp. 93-104 ◽  
Author(s):  
Montserrat Lara-Velazquez ◽  
Rawan Al-kharboosh ◽  
Luis Prieto ◽  
Paula Schiapparelli ◽  
Alfredo Quiñones-Hinojosa
Keyword(s):  
Stem Cell ◽  
Cell Migration ◽  
Brain Tumor ◽  
Tumor Stem Cell ◽  
Brain Tumor Stem Cell ◽  
Stem Cell Migration

ADAM17 promotes U87 glioblastoma stem cell migration and invasion

2013 ◽  
Vol 1538 ◽  
pp. 151-158 ◽  
Author(s):  
Xiangrong Chen ◽  
Lei Chen ◽  
Junyan Chen ◽  
Weipeng Hu ◽  
Hongzhi Gao ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Migration ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Stem Cell Migration ◽  
Glioblastoma Stem Cell

scholarly journals Semaphorin 3A mediated brain tumor stem cell proliferation and invasion in EGFRviii mutant gliomas

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Dominique M. O. Higgins ◽  
Maisel Caliva ◽  
Mark Schroeder ◽  
Brett Carlson ◽  
Pavan S. Upadhyayula ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cell ◽  
Brain Tumor ◽  
Propidium Iodide ◽  
Tumor Stem Cell ◽  
Semaphorin 3A ◽  
Brain Tumor Stem Cell ◽  
Proliferation And Invasion ◽  
Invasion Assays

Abstract Background Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults, with a median survival of approximately 15 months. Semaphorin 3A (Sema3A), known for its axon guidance and antiangiogenic properties, has been implicated in GBM growth. We hypothesized that Sema3A directly inhibits brain tumor stem cell (BTSC) proliferation and drives invasion via Neuropilin 1 (Nrp1) and Plexin A1 (PlxnA1) receptors. Methods GBM BTSC cell lines were assayed by immunostaining and PCR for levels of Semaphorin 3A (Sema3A) and its receptors Nrp1 and PlxnA1. Quantitative BrdU, cell cycle and propidium iodide labeling assays were performed following exogenous Sema3A treatment. Quantitative functional 2-D and 3-D invasion assays along with shRNA lentiviral knockdown of Nrp1 and PlxnA1 are also shown. In vivo flank studies comparing tumor growth of knockdown versus control BTSCs were performed. Statistics were performed using GraphPad Prism v7. Results Immunostaining and PCR analysis revealed that BTSCs highly express Sema3A and its receptors Nrp1 and PlxnA1, with expression of Nrp1 in the CD133 positive BTSCs, and absence in differentiated tumor cells. Treatment with exogenous Sema3A in quantitative BrdU, cell cycle, and propidium iodide labeling assays demonstrated that Sema3A significantly inhibited BTSC proliferation without inducing cell death. Quantitative functional 2-D and 3-D invasion assays showed that treatment with Sema3A resulted in increased invasion. Using shRNA lentiviruses, knockdown of either NRP1 or PlxnA1 receptors abrogated Sema3A antiproliferative and pro-invasive effects. Interestingly, loss of the receptors mimicked Sema3A effects, inhibiting BTSC proliferation and driving invasion. Furthermore, in vivo studies comparing tumor growth of knockdown and control infected BTSCs implanted into the flanks of nude mice confirmed the decrease in proliferation with receptor KD. Conclusions These findings demonstrate the importance of Sema3A signaling in GBM BTSC proliferation and invasion, and its potential as a therapeutic target.

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