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 Induction of Stem Cell Like Cells from Mouse Embryonic Fibroblast by Short-Term Shear Stress and Vitamin C

2021 ◽  
Vol 11 (4) ◽  
pp. 1941
Author(s):  
Seungmin Yeom ◽  
Myung Chul Lee ◽  
Shambhavi Pandey ◽  
Jaewoon Lim ◽  
Sangbae Park ◽  
...  
Keyword(s):  
Stem Cells ◽  
Shear Stress ◽  
Stem Cell ◽  
Vitamin C ◽  
Suspension Culture ◽  
Small Molecules ◽  
Tumor Development ◽  
Embryonic Stem ◽  
Short Term ◽  
External Stimuli

Induced pluripotent stem cells (iPSCs) are a good medicine source because of their potential to differentiate into various tissues or cells. However, traditionally, iPSCs made by specific transgenes and virus vectors are not appropriate for clinical use because of safety concerns and risk of tumor development. The goal of this research was to develop an alternative method for reprogramming, using small molecules and external stimuli. Two groups were established: short-term shear stress (STSS) under suspension culture and a combination of short-term shear stress and vitamin C (SSVC) under suspension culture. For STSS, the pipetting was carried out for cells twice per day for 2 min for 14 days in the embryonic stem cell (ES) medium. In the case of SSVC, the procedure was the same as for STSS however, its ES medium included 10 µM of vitamin C. After 14 days, all spheroids were picked and checked for pluripotency by ALP (alkaline phosphatase) assay and immunocytochemistry. Both groups partially showed the characteristics of stem cells but data demonstrated that the spheroids under shear stress and vitamin C had improved stem cell-like properties. This research showed the possibility of external stimuli and small molecules to reprogram the somatic cells without the use of transgenes.

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.

scholarly journals Hedgehog signaling maintains a tumor stem cell compartment in multiple myeloma

2007 ◽  
Vol 104 (10) ◽  
pp. 4048-4053 ◽  
Author(s):  
C. D. Peacock ◽  
Q. Wang ◽  
G. S. Gesell ◽  
I. M. Corcoran-Schwartz ◽  
E. Jones ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Stem Cell ◽  
Hedgehog Signaling ◽  
Tumor Stem Cell ◽  
Cell Compartment ◽  
Stem Cell Compartment
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