A172 and T98G cell lines characteristics

Киселева, Л. Н.; Карташев, А. В.; Vartanyan, N. L.; Pinevich, A. A.; Самойлович, М. П.

doi:10.1134/s1990519x16050072

Cited by 35 publications

(20 citation statements)

References 28 publications

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“…To confirm these observations, we performed a comparative analysis of energy metabolism in human hepatocellular carcinoma cells (HepG2) and a human glioblastoma cell line (T98G) (Figure 1B,C). The HepG2 cell line possesses appropriate characteristics for in vitro experiments involving energy imbalance and induction of oxidative stress [12], and the T98G cell line is routinely utilized as an experimental standard for improving therapeutic strategies for GBM [51]. A high-resolution, comparative analysis of oxygen consumption by intact cells revealed that HepG2 cells rely on mitochondrial respiration, and that their utilization of oxygen is instant and more rapid than that by T98G cells (Figure 1B).…”

Section: Discussionmentioning

confidence: 99%

Implications of Oxidative Stress in Glioblastoma Multiforme Following Treatment with Purine Derivatives

et al. 2021

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Recently, small compound-based therapies have provided new insights into the treatment of glioblastoma multiforme (GBM) by inducing oxidative impairment. Kinetin riboside (KR) and newly designed derivatives (8-azaKR, 7-deazaKR) selectively affect the molecular pathways crucial for cell growth by interfering with the redox status of cancer cells. Thus, these compounds might serve as potential alternatives in the oxidative therapy of GBM. The increased basal levels of reactive oxygen species (ROS) in GBM support the survival of cancer cells and cause drug resistance. The simplest approach to induce cell death is to achieve the redox threshold and circumvent the antioxidant defense mechanisms. Consequently, cells become more sensitive to oxidative stress (OS) caused by exogenous agents. Here, we investigated the effect of KR and its derivatives on the redox status of T98G cells in 2D and 3D cell culture. The use of spheroids of T98G cells enabled the selection of one derivative—7-deazaKR—with comparable antitumor activity to KR. Both compounds induced ROS generation and genotoxic OS, resulting in lipid peroxidation and leading to apoptosis. Taken together, these results demonstrated that KR and 7-deazaKR modulate the cellular redox environment of T98G cells, and vulnerability of these cells is dependent on their antioxidant capacity.

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Section: Discussionmentioning

confidence: 99%

Implications of Oxidative Stress in Glioblastoma Multiforme Following Treatment with Purine Derivatives

et al. 2021

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“…3) in A172 cells, but not in two other cell lines, T98G and U373MG. A172 cells are monomorphic and fibroblast-like whereas T98G cells are polymorphic, fibroblast-like and polygonal (28). U373MG cells have pleomorphic features (29).…”

Section: Discussionmentioning

confidence: 99%

Epimedium koreanum Nakai inhibits PMA-induced cancer cell migration and invasion by modulating NF-κB/MMP-9 signaling in monomorphic malignant human glioma cells

et al. 2017

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Previously, we showed that the herbal extract EYK (Epimedium koreanum Nakai) can regulate the immune response. Other studies showed that EYK has beneficial effects in human lung cancer, angiogenesis and Alzheimer's disease (AD). However, it remains unknown whether EYK can affect cancer cell migration and invasion in human brain cancer cell lines. In the present study, we found that pre- or post-treatment with EYK inhibited phorbol 12-myristate 13-acetate (PMA)-induced cancer cell migration and invasion in A172 cells, but not in U373MG or T98G cells. Additionally, pre- or post-treatment with PMA followed by EYK decreased MMP-9 activity in A172 cells. Moreover, treatment with a NF-κB inhibitor significantly decreased cell migration in A172 cells pre- or post-treated with EYK and PMA, suggesting that EYK requires NF-κB to alter cancer cell migration. Either pre- or post-treatment with EYK significantly decreased NF-κB nuclear translocation in comparison with PMA treatment. Taken together, our results suggest that EYK suppresses PMA-induced cancer cell migration in monomorphic malignant human glioma cells by downregulating the NF-κB pathway and decreasing MMP-9 activity.

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“…Glioblastoma can be molecularly classified into proneural, neural, classical, and mesenchymal types according to The Cancer Genome Atlas (TCGA) 36 . We use two glioblastoma cell models, T98G and U-251MG, which are both of caucasian male origin and classified as mesenchymal type with p53 mutant genotype 37,38 . The adhesion and electrotaxis of T98G and U-251MG glioblastoma cell lines on various ECMs are tested in a double-layer hybrid multiple electric field chip (HMEFC) based on the hybrid PMMA/PDMS design approach 17 (Supplementary TABLE. S.1).…”

Section: B Glioblastoma Electrotaxis Requires Optimal Laminin-contaimentioning

confidence: 99%

“…Both T98G cells and U-251MG cells are categorized as mesenchymal type glioblastoma 37,38 , however, their electrotactic responses are completely different. Similar results are reported in the electrotaxis of glioblastoma cells and spheroids 15,16,19,39 and lung adenocarcinoma 51 , showing that although molecular and surface marker makeups of the cell lines are similar, their electrotaxis responses can be completely different.…”

Section: Electrotaxis Behavior May Reflect the Heterogeneity Of Glmentioning

confidence: 99%

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

Tsai

IJspeert

Shen

2020

Preprint

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Transformed astrocytes in the most aggressive form cause glioblastoma, the most common cancer in central nervous system with high mortality. The physiological electric field by neuronal local field potentials and tissue polarity may guide the infiltration of glioblastoma cells through the electrotaxis process. However, microenvironments with multiplex gradients are difficult to create. In this work, we have developed a hybrid microfluidic platform to study glioblastoma electrotaxis in controlled microenvironments with high throughput quantitative analysis by a machine learning-powered single cell tracking software. By equalizing the hydrostatic pressure difference between inlets and outlets of the microchannel, uniform single cells can be seeded reliably inside the microdevice. The electrotaxis of two glioblastoma models, T98G and U-251MG, require optimal laminin-containing extracellular matrix and exhibits opposite directional and electro-alignment tendencies. Calcium signaling is a key contributor in glioblastoma pathophysiology but its role in glioblastoma electrotaxis is still an open question. Anodal T98G electrotaxis and cathodal U-251MG electrotaxis require the presence of extracellular calcium cations. U-251MG electrotaxis is dependent on the P/Q-type voltage-gated calcium channel (VGCC) and T98G is dependent on the R-type VGCC. U-251MG and T98G electrotaxis are also mediated by A-type (rapidly inactivating) voltage-gated potassium channels and acidsensing sodium channels. The involvement of multiple ion channels suggests that the glioblastoma electrotaxis is complex and patient-specific ion channel expression can be critical to develop personalized therapeutics to fight against cancer metastasis. The hybrid microfluidic design and machine learning-powered single cell analysis provide a simple and flexible platform for quantitative investigation of complicated biological systems.

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A172 and T98G cell lines characteristics

Cited by 35 publications

References 28 publications

Implications of Oxidative Stress in Glioblastoma Multiforme Following Treatment with Purine Derivatives

Implications of Oxidative Stress in Glioblastoma Multiforme Following Treatment with Purine Derivatives

Epimedium koreanum Nakai inhibits PMA-induced cancer cell migration and invasion by modulating NF-κB/MMP-9 signaling in monomorphic malignant human glioma cells

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

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