BMP7 Induces Dormancy of Prostatic Tumor Stem Cell in Bone

2013 ◽  
Author(s):  
Fei Xing
Keyword(s):  
Stem Cell ◽  
Tumor Stem Cell ◽  
Prostatic Tumor

Abstract 5762: Role of BMP7 in dormancy and recurrence of prostatic tumor stem cell in the bone metastasis

2010 ◽  
Author(s):  
Aya Kobayashi ◽  
Hiroshi Okuda ◽  
Eiji Furuta ◽  
Puspa R. Pandey ◽  
Misako Watabe ◽  
...  
Keyword(s):  
Stem Cell ◽  
Bone Metastasis ◽  
Tumor Stem Cell ◽  
Prostatic Tumor

Vitamin C deficient reduces proliferation in a human periventricular tumor stem cell‐derived glioblastoma model

2021 ◽  
Author(s):  
Nery Jara ◽  
Eder Ramirez ◽  
Luciano Ferrada ◽  
Katterine Salazar ◽  
Francisca Espinoza ◽  
...  
Keyword(s):  
Stem Cell ◽  
Vitamin C ◽  
Tumor 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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