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Life
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Molecular and Cellular Biology of Glioblastoma
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Molecular and Cellular Biology of Glioblastoma

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 8695

Special Issue Editors

Dr. Tsung-I Hsu

E-Mail Website
Guest Editor
Ph.D. Program in Medical Neuroscience, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
Interests: glioblastoma; drug resistance; neurosteroids; Sp1
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jian-Ying Chuang

E-Mail Website
Guest Editor
Ph.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
Interests: neuroprotection; brain cancer stem cell; drug addiction; tumor heterogeneity; microenvironment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The medical care for cancer and patients’ prognoses has greatly improved in the last 3 decades. The survival for most cancer types, including melanoma, prostate cancer and breast cancer, is also greatly increased. However, some types of cancers still exhibit very little improvement since the early 1970s, including pancreas and brain tumors. Particularly, glioblastoma, derived from glial and astrocytes, accounts for most brain tumors and is the most malignant in all kinds of brain tumors. The median survival of glioblastoma patients is only 14~16 months after first diagnosis, medical surgery, chemo- and radiotherapies. The standard treatment for glioblastoma is temozolomide (TMZ)-mediated chemotherapy conjugated with radiotherapy (CCRT) after surgery. Unfortunately, the efficacy of CCRT is always restricted within a short period due to the high prevalence of tumor recurrence. A recurrent tumor always exhibits higher and higher tolerance in response to TMZ treatment cycle, leading to drug resistance, which is the main obstacle in improving patients’ prognosis. In the last decade, O6-methylguanine-DNA methyltransferase (MGMT)-mediated DNA repair was thought of as the culprit for drug resistance in glioblastoma. However, recent reports indicate that MGMT accounts for 40% of recurrent glioblastoma, and MGMT-negative tumors are still able to develop drug resistance through enhancing DNA repair capacity, enriching cancer stem cells, and increasing neurosteroids’ synthesis. However, it is still lacking an effective approach or a biomarker to predict therapeutic efficacy, and to estimate the prevalence of tumor recurrence in glioblastoma. In addition, the blood–brain barrier protects brain tissue, and protects brain tumors against chemotherapeutic drugs, further increasing the difficulty in drug discovery for glioblastoma. Therefore, we still have to make numerous efforts in dissecting important mechanisms and in investigating novel biomarkers underlying the acquirement of chemotherapeutic resistance by glioblastoma.

Dr. Tsung-I Hsu
Prof. Dr. Jian-Ying Chuang
Guest Editors

Manuscript Submission Information

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Keywords

  • glioblastoma
  • temozolomide resistance
  • recurrence

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Published Papers (3 papers)

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17 pages, 1473 KiB  
Article
Galvanotactic Migration of Glioblastoma and Brain Metastases Cells
by Falko Lange, Jakob Venus, Daria Shams Esfand Abady, Katrin Porath, Anne Einsle, Tina Sellmann, Valentin Neubert, Gesine Reichart, Michael Linnebacher, Rüdiger Köhling and Timo Kirschstein
Life 2022, 12(4), 580; https://doi.org/10.3390/life12040580 - 14 Apr 2022
Cited by 6 | Viewed by 2773
Abstract
Galvanotaxis, the migration along direct current electrical fields, may contribute to the invasion of brain cancer cells in the tumor-surrounding tissue. We hypothesized that pharmacological perturbation of the epidermal growth factor (EGF) receptor and downstream phosphatidylinositol 3-kinase (PI3K)/AKT pathway prevent galvanotactic migration. In [...] Read more.
Galvanotaxis, the migration along direct current electrical fields, may contribute to the invasion of brain cancer cells in the tumor-surrounding tissue. We hypothesized that pharmacological perturbation of the epidermal growth factor (EGF) receptor and downstream phosphatidylinositol 3-kinase (PI3K)/AKT pathway prevent galvanotactic migration. In our study, patient-derived glioblastoma and brain metastases cells were exposed to direct current electrical field conditions. Velocity and direction of migration were estimated. To determine the effects of EGF receptor antagonist afatinib and AKT inhibitor capivasertib, assays of cell proliferation, apoptosis and immunoblot analyses were performed. Both inhibitors attenuated cell proliferation in a dose-dependent manner and induced apoptosis. We found that most of the glioblastoma cells migrated preferentially in an anodal direction, while brain metastases cells were unaffected by direct current stimulations. Afatinib presented only a mild attenuation of galvanotaxis. In contrast, capivasertib abolished the migration of glioblastoma cells without genetic alterations in the PI3K/AKT pathway, but not in cells harboring PTEN mutation. In these cells, an increase in the activation of ERK1/2 may in part substitute the inhibition of the AKT pathway. Overall, our data demonstrate that glioblastoma cells migrate in the electrical field and the PI3K/AKT pathway was found to be highly involved in galvanotaxis. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Glioblastoma)
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11 pages, 2377 KiB  
Article
Magnolol Induces the Extrinsic/Intrinsic Apoptosis Pathways and Inhibits STAT3 Signaling-Mediated Invasion of Glioblastoma Cells
by Po-Fu Yueh, Yuan-Hao Lee, Chun-Yu Fu, Chun-Bin Tung, Fei-Ting Hsu and Keng-Li Lan
Life 2021, 11(12), 1399; https://doi.org/10.3390/life11121399 - 14 Dec 2021
Cited by 10 | Viewed by 2688
Abstract
Glioblastoma multiforme (GBM) is the most common form of malignant brain tumor, with poor prognosis; the efficacy of current standard therapy for GBM remains unsatisfactory. Magnolol, an herbal medicine from Magnolia officinalis, exhibited anticancer properties against many types of cancers. However, whether [...] Read more.
Glioblastoma multiforme (GBM) is the most common form of malignant brain tumor, with poor prognosis; the efficacy of current standard therapy for GBM remains unsatisfactory. Magnolol, an herbal medicine from Magnolia officinalis, exhibited anticancer properties against many types of cancers. However, whether magnolol suppresses GBM progression as well as its underlying mechanism awaits further investigation. In this study, we used the MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay, apoptosis marker analysis, transwell invasion and wound-healing assays to identify the effects of magnolol on GBM cells. We also validated the potential targets of magnolol on GBM with the GEPIA (Gene Expression Profiling Interactive Analysis) and Western blotting assay. Magnolol was found to trigger cytotoxicity and activate extrinsic/intrinsic apoptosis pathways in GBM cells. Both caspase-8 and caspase-9 were activated by magnolol. In addition, GEPIA data indicated the PKCδ (Protein kinase C delta)/STAT3 (Signal transducer and activator of transcription 3) signaling pathway as a potential target of GBM. Magnolol effectively suppressed the phosphorylation and nuclear translocation of STAT3 in GBM cells. Meanwhile, tumor invasion and migration ability and the associated genes, including MMP-9 (Matrix metalloproteinase-9) and uPA (Urokinase-type plasminogen activator), were all diminished by treatment with magnolol. Taken together, our results suggest that magnolol-induced anti-GBM effect may be associated with the inactivation of PKCδ/STAT3 signaling transduction. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Glioblastoma)
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15 pages, 4313 KiB  
Article
Enhanced Microglia Activation and Glioma Tumor Progression by Inflammagen Priming in Mice with Tumor Necrosis Factor Receptor Type 2 Deficiency
by Chih-Kai Liao, Kuan-Min Fang, Hui-Ting Huang, Wen-Ruei Chang, Chao-Chi Chuang and Shun-Fen Tzeng
Life 2021, 11(9), 961; https://doi.org/10.3390/life11090961 - 14 Sep 2021
Cited by 4 | Viewed by 2445
Abstract
Despite the fact that accumulation of microglia, the resident macrophages of the central nervous system (CNS) are the main feature of glioblastoma, the role of microglia in the progression of glioma is still arguable. Based on the correlation of inflammation with tumor progression, [...] Read more.
Despite the fact that accumulation of microglia, the resident macrophages of the central nervous system (CNS) are the main feature of glioblastoma, the role of microglia in the progression of glioma is still arguable. Based on the correlation of inflammation with tumor progression, in this study, we attempt to determine if peripheral inflammation aggravates glioma expansion and the activation of microglia associated with the tumor. Experimental animals were administered intraperitoneally by inflammagen lipopolysaccharide (LPS) for 7 days (LPS priming) before intracerebral implantation of glioma cells. Moreover, a reduced level of tumor necrosis factor receptor type 2 (TNFR2) that is restricted to immune cells, neurons, and microglia has been found in patients with glioblastoma through the clinic analysis of monocyte receptor expression. Thus, in addition to wildtype (WT) mice, heterogeneous TNFR2 gene deficiency (TNFR2+/−) mice and homogeneous TNFR2 gene knockout (TNFR2−/−) mice were used in this study. The results show that peripheral challenge by LPS, Iba1+- or CD11b+-microglia increase in numbers in the cortex and hippocampus of TNFR2−/− mice, when compared to WT or TNFR2+/− mice. We further conducted the intracerebral implantation of rodent glioma cells into the animals and found that the volumes of tumors formed by rat C6 glioma cells or mouse GL261 glioma cells were significantly larger in the cortex of TNFR2−/− mice when compared to that measured in LPS-primed WT or LPS-primed TNFR2+/− mice. Ki67+-cells were exclusively clustered in the tumor of LPS-primed TNFR2−/− mice. Microglia were also extensively accumulated in the tumor formed in LPS-primed TNFR2−/− mice. Accordingly, our findings demonstrate that aggravation of microglia activation by peripheral inflammatory challenge and a loss of TNFR2 function might lead to the promotion of glioma growth. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Glioblastoma)
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