The shaping of invasive glioma phenotype by the ubiquitin–proteasome system

Vlachostergios, Panagiotis J.; Voutsadakis, Ioannis A.; Papandreou, Christos N.

doi:10.3109/15419061.2013.833192

Cited by 4 publications

(3 citation statements)

References 63 publications

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“…In this regard, Vlachostergios et al . [ 206 ] compile a set of proteins participating in motility and invasion of tumors, including gliomas, whose regulation would be determined through UPS, presenting a group of potential targets many of which are overexpressed.…”

Section: Remarksmentioning

confidence: 99%

The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme

Maksoud

2021

Mol Neurobiol

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Gliomas constitute the most frequent tumors of brain. High-grade gliomas are characterized by a poor prognosis caused by a set of attributes making treatment difficult, such as heterogeneity and cell infiltration. Additionally, there is a subgroup of glioma cells with properties similar to stem cells responsible for tumor recurrence after treatment. Since proteasomal degradation regulates multiple cellular processes, any mutation causing disturbances in the function or expression of its elements can lead to various disorders such as cancer. Several studies have focused on protein degradation modulation as a mechanism of glioma control. The ubiquitin proteasome system is the main mechanism of cellular proteolysis that regulates different events, intervening in pathological processes with exacerbating or suppressive effects on diseases. This review analyzes the role of proteasomal degradation in gliomas, emphasizing the elements of this system that modulate different cellular mechanisms in tumors and discussing the potential of distinct compounds controlling brain tumorigenesis through the proteasomal pathway.

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Section: Remarksmentioning

confidence: 99%

The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme

Maksoud

2021

Mol Neurobiol

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“…Proteasome inhibition can result in the induction of unfolded protein response (UPR) and endoplasmic reticulum (ER) stress, and thus, it offers a way to target GBM. 133,134 Bortezomib (a proteasome inhibitor) induces ER stress and UPR, which contributed to significantly enhanced oHSV (34.5ENVE) replication and synergistic killing of glioma cells. 135 HSP90 was found to be the most critical UPR for increased oHSV replication.…”

Section: Inhibition Of Proteasomementioning

confidence: 99%

The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment

Nguyen¹,

Saha²

2021

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Glioblastoma (GBM) is a lethal primary malignant brain tumor with no current effective treatments. The recent emergence of immuno-virotherapy and FDA approval of T-VEC have generated a great expectation towards oncolytic herpes simplex viruses (oHSVs) as a promising treatment option for GBM. Since the generation and testing of the first genetically engineered oHSV in glioma in the early 1990s, oHSV-based therapies have shown a long way of great progress in terms of anti-GBM efficacy and safety, both preclinically and clinically. Here, we revisit the literature to understand the recent advancement of oHSV in the treatment of GBM. In addition, we discuss current obstacles to oHSV-based therapies and possible strategies to overcome these pitfalls.

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“…Cancer cells have a high turnover of proteins due to translation of dysfunctional proteins brought on by their rapid growth (28). Furthermore, key signalling pathways in GBM converge upon and involve the 26S proteasome (29).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of glioblastoma cell proliferation, migration and invasion by the proteasome antagonist carfilzomib

et al. 2016

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Glioblastoma multiforme is the most aggressive and lethal tumor of the central nervous system with limited treatment strategies on offer, and as such the identification of effective novel therapeutic agents is paramount. To examine the efficacy of proteasome inhibitors, we tested bortezomib, carfilzomib, nafamostat mesylate, gabexate mesylate and acetylsalicylic acid on glioblastoma cell viability, migration and invasion. Both bortezomib and carfilzomib produced significant reduction of cell viability, while nafamostat mesylate, gabexate mesylate and acetylsalicylic acid did not. Subsequent testing showed that carfilzomib significantly reduced cell viability at nM concentrations. Carfilzomib also reduced cell migration, secretion and activation of MMP2 and also cell invasion of all four glioblastoma cells tested. In summary, carfilzomib represents a novel, yet FDA-approved agent for the treatment of glioblastoma multiforme.

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The shaping of invasive glioma phenotype by the ubiquitin–proteasome system

Cited by 4 publications

References 63 publications

The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme

The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme

The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment

Inhibition of glioblastoma cell proliferation, migration and invasion by the proteasome antagonist carfilzomib

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