Isolation and Culture of Primary Glioblastoma Cells from Human Tumor Specimens

2014 ◽  
pp. 263-275 ◽  
Author(s):  
Sascha Seidel ◽  
Boyan K. Garvalov ◽  
Till Acker
Keyword(s):  
Human Tumor ◽  
Glioblastoma Cells ◽  
Primary Glioblastoma

scholarly journals Inhibition of Gap Junctions Sensitizes Primary Glioblastoma Cells for Temozolomide

Cancers ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 858 ◽  
Author(s):  
Anna-Laura Potthoff ◽  
Dieter Henrik Heiland ◽  
Bernd O. Evert ◽  
Filipe Rodrigues Almeida ◽  
Simon P. Behringer ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Glioblastoma Cells ◽  
Primary Glioblastoma ◽  
Blood Brain ◽  
Elevated Activity ◽  
Essential Contribution ◽  
Gap Junction Inhibitor

Gap junctions have recently been shown to interconnect glioblastoma cells to a multicellular syncytial network, thereby allowing intercellular communication over long distances as well as enabling glioblastoma cells to form routes for brain microinvasion. Against this backdrop gap junction-targeted therapies might provide for an essential contribution to isolate cancer cells within the brain, thus increasing the tumor cells’ vulnerability to the standard chemotherapeutic agent temozolomide. By utilizing INI-0602—a novel gap junction inhibitor optimized for crossing the blood brain barrier—in an oncological setting, the present study was aimed at evaluating the potential of gap junction-targeted therapy on primary human glioblastoma cell populations. Pharmacological inhibition of gap junctions profoundly sensitized primary glioblastoma cells to temozolomide-mediated cell death. On the molecular level, gap junction inhibition was associated with elevated activity of the JNK signaling pathway. With the use of a novel gap junction inhibitor capable of crossing the blood–brain barrier—thus constituting an auspicious drug for clinical applicability—these results may constitute a promising new therapeutic strategy in the field of current translational glioblastoma research.

scholarly journals CCR5-Mediated Signaling is Involved in Invasion of Glioblastoma Cells in Its Microenvironment

2020 ◽  
Vol 21 (12) ◽  
pp. 4199
Author(s):  
Metka Novak ◽  
Miha Koprivnikar Krajnc ◽  
Barbara Hrastar ◽  
Barbara Breznik ◽  
Bernarda Majc ◽  
...  
Keyword(s):  
Stem Cells ◽  
Low Grade ◽  
Glioblastoma Cells ◽  
Ccr5 Gene ◽  
Glioblastoma Stem Cells ◽  
Primary Glioblastoma ◽  
Tissue Sections ◽  
Stromal Microenvironment ◽  
Close Proximity

The chemokine CCL5/RANTES is a versatile inflammatory mediator, which interacts with the receptor CCR5, promoting cancer cell interactions within the tumor microenvironment. Glioblastoma is a highly invasive tumor, in which CCL5 expression correlates with shorter patient survival. Using immunohistochemistry, we identified CCL5 and CCR5 in a series of glioblastoma samples and cells, including glioblastoma stem cells. CCL5 and CCR5 gene expression were significantly higher in a cohort of 38 glioblastoma samples, compared to low-grade glioma and non-cancerous tissues. The in vitro invasion of patients-derived primary glioblastoma cells and glioblastoma stem cells was dependent on CCL5-induced CCR5 signaling and is strongly inhibited by the small molecule CCR5 antagonist maraviroc. Invasion of these cells, which was enhanced when co-cultured with mesenchymal stem cells (MSCs), was inhibited by maraviroc, suggesting that MSCs release CCR5 ligands. In support of this model, we detected CCL5 and CCR5 in MSC monocultures and glioblastoma-associated MSC in tissue sections. We also found CCR5 expressing macrophages were in close proximity to glioblastoma cells. In conclusion, autocrine and paracrine cross-talk in glioblastoma and, in particular, glioblastoma stem cells with its stromal microenvironment, involves CCR5 and CCL5, contributing to glioblastoma invasion, suggesting the CCL5/CCR5 axis as a potential therapeutic target that can be targeted with repositioned drug maraviroc.

scholarly journals Induction of senescence in primary glioblastoma cells by serum and TGFβ

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ritesh Kumar ◽  
Alexander Gont ◽  
Theodore J. Perkins ◽  
Jennifer E. L. Hanson ◽  
Ian A. J. Lorimer
Keyword(s):  
Glioblastoma Cells ◽  
Primary Glioblastoma

Delivery and cytotoxicity of doxorubicin and temozolomide to primary glioblastoma cells using gold nanospheres and gold nanorods

2016 ◽  
Vol 8 (1) ◽  
Author(s):  
Jyoti Verma ◽  
Henk A. Van Veen ◽  
Sumit Lal ◽  
Cornelis J.F. Van Noorden
Keyword(s):  
Gold Nanoparticles ◽  
Cell Cultures ◽  
Gold Nanorods ◽  
Silica Coating ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Gold Nanospheres ◽  
Primary Glioblastoma ◽  
Direct Delivery

AbstractNanoparticles with coating entrapping a chemotherapeutic drug for delivery have not been tested for their cytotoxic effects in in-vitro glioblastoma cell cultures to increase treatment efficacy. Therefore, we synthesized silica-coated gold nanorods and gold nanospheres that were loaded with doxorubicin or temozolomide. The morphology of the nanoparticles was characterized using transmission electron microscopy (TEM), the molecular structure was characterized using infrared spectroscopy and in vitro efficacy was determined using glioblastoma cell cultures. TEM analysis showed that gold nanorods had a length of 49–65 nm and a diameter of 8.5–14 nm whereas gold nanospheres had a diameter of 9.5–37 nm. Infrared spectroscopy of doxorubicin and temozolomide and the silica coating revealed molecular fingerprints such as bending, stretching and vibrations of chemical bonds that confirmed the presence of silica coating and drug loading of the gold nanoparticles. In the biological assessment of the effects of drug-loaded gold nanoparticles on primary glioblastoma cell cultures, cytotoxicity, viability and the ratio of cyototoxicity and viability were used as parameters to analyze the effects on the cells of drug delivery via gold nanoparticles on the cells. Our data suggest that doxorubicin in the concentration range of 0.12–3.16 μM when delivered using both gold nanorods and nanospheres induced a 3.8–5.5-fold increased cytotoxicity in comparison to direct delivery. Temozolomide in the concentration range of 4.6–115 μM when delivered by either type of gold nanoparticles induced a 2–4-fold increased cytotoxicity in comparison to direct delivery. Nanospheres were more effective in delivery and cytotoxicity of doxorubicin and temozolomide to glioblastoma cells than gold nanorods. Our data suggest that gold nanoparticles and in particular gold nanospheres are more effective in delivery of doxorubicin and temozolomide to primary glioblastoma cells in culture than direct delivery.

scholarly journals Wild‑type IDH1 affects cell migration by modulating the PI3K/AKT/mTOR pathway in primary glioblastoma cells

2020 ◽  
Vol 22 (3) ◽  
pp. 1949-1957 ◽  
Author(s):  
Xiaopeng Shen ◽  
Shen Wu ◽  
Jingyi Zhang ◽  
Meng Li ◽  
Feng Xu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Mtor Pathway ◽  
Wild Type ◽  
Glioblastoma Cells ◽  
Primary Glioblastoma

scholarly journals Brusatol Inhibits Proliferation and Invasion of Glioblastoma by Down-Regulating the Expression of ECM1

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhang’an Dai ◽  
Lin Cai ◽  
Yingyu Chen ◽  
Silu Wang ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Matrix Protein ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Herbal Extract ◽  
Extracellular Matrix Protein ◽  
Glioblastoma Cells ◽  
Primary Glioblastoma ◽  
Proliferation And Invasion

Brusatol (Bru), a Chinese herbal extract, has a variety of anti-tumor effects. However, little is known regarding its role and underlying mechanism in glioblastoma cells. Here, we found that Bru could inhibit the proliferation of glioblastoma cells in vivo and in vitro. Besides, it also had an inhibitory effect on human primary glioblastoma cells. RNA-seq analysis indicated that Bru possibly achieved these effects through inhibiting the expression of extracellular matrix protein 1 (ECM1). Down-regulating the expression of ECM1 via transfecting siRNA could weaken the proliferation and invasion of glioblastoma cells and promote the inhibitory effect of Bru treatment. Lentivirus-mediated overexpression of ECM1 could effectively reverse this weakening effect. Our findings indicated that Bru could inhibit the proliferation and invasion of glioblastoma cells by suppressing the expression of ECM1, and Bru might be a novel effective anticancer drug for glioblastoma cells.

scholarly journals Mitochondria transfer from tumor-activated stromal cells (TASC) to primary Glioblastoma cells

2020 ◽  
Vol 533 (1) ◽  
pp. 139-147
Author(s):  
Céline Salaud ◽  
Arturo Alvarez-Arenas ◽  
Fanny Geraldo ◽  
Juan Belmonte-Beitia ◽  
Gabriel F. Calvo ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Glioblastoma Cells ◽  
Primary Glioblastoma ◽  
Mitochondria Transfer
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