Dual functions of <scp>ARP</scp>101 in targeting membrane type‐1 matrix metalloproteinase: Impact on U87 glioblastoma cell invasion and autophagy signaling

Desjarlais, Michel; Annabi, Borhane

doi:10.1111/cbdd.13410

Cited by 4 publications

(6 citation statements)

References 55 publications

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“…A series of studies have elucidated the mechanism by which MT1-MMP promotes autophagy and induced autophagic death in tumor cells. MT1-MMP expression was increased in ConA-activated glioblastoma cells, and the expression of autophagy-related markers Bcl-2, ATG9, and LC3 was also enhanced, with autophagosome formation; after silencing of the MT1-MMP genes by SiRNA, the expression of these genes was decreased and autophagy was inhibited ( Pratt et al, 2012 ; Pratt et al, 2016 ; Desjarlais and Annabi, 2019 ).…”

Section: Autophagymentioning

confidence: 99%

The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors

Zhang²,

Mao

et al. 2022

Front. Genet.

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Tumor is one of the important factors affecting human life and health in today’s world, and scientists have studied it extensively and deeply, among which autophagy and JAK/STAT3 signaling pathway are two important research directions. The JAK/STAT3 axis is a classical intracellular signaling pathway that assumes a key role in the regulation of cell proliferation, apoptosis, and vascular neogenesis, and its abnormal cell signaling and regulation are closely related to the occurrence and development of tumors. Therefore, the JAK/STAT3 pathway in tumor cells and various stromal cells in their microenvironment is often considered as an effective target for tumor therapy. Autophagy is a process that degrades cytoplasmic proteins and organelles through the lysosomal pathway. It is a fundamental metabolic mechanism for intracellular degradation. The mechanism of action of autophagy is complex and may play different roles at various stages of tumor development. Altered STAT3 expression has been found to be accompanied by the abnormal autophagy activity in many oncological studies, and the two may play a synergistic or antagonistic role in promoting or inhibiting the occurrence and development of tumors. This article reviews the recent advances in autophagy and its interaction with JAK/STAT3 signaling pathway in the pathogenesis, prevention, diagnosis, and treatment of tumors.

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Section: Autophagymentioning

confidence: 99%

The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors

Zhang²,

Mao

et al. 2022

Front. Genet.

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“…Sinomenine hydrochloride, a bioactive alkaloid, is able to decrease invasion of glioblastoma cells through activation of autophagy and suppression of NFkB activation with subsequent decrease in MMP-2/MMP-9 level [135]. At last, the actin-related protein 10 (ARP10) has been shown to inhibit MMP-14 auto-proteolytic processing, and consequently MMP-2 activation, in addition to trigger autophagy-mediated cell death [136]. These recent studies confirm that MMPs still represent promising targets in glioblastoma and that investigations elucidating their mediated mechanisms would still be beneficial for development of novel therapeutics.…”

Section: Mmp-targeted Therapies In Glioblastomamentioning

confidence: 99%

Extracellular proteolysis in glioblastoma progression and therapeutics

Quesnel

Karagiannis

Filippou

2020

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Gliomas encompass highly invasive primary central nervous system (CNS) tumours of glial cell origin with an often-poor clinical prognosis. Of all gliomas, glioblastoma is the most aggressive form of primary brain cancer. Current treatments in glioblastoma are insufficient due to the invasive nature of brain tumour cells, which typically results in local tumour recurrence following treatment. The latter represents the most important cause of mortality in glioblastoma and underscores the necessity for an in-depth understanding of the underlying mechanisms. Interestingly, increased synthesis and secretion of several proteolytic enzymes within the tumour microenvironment, such as matrix metalloproteinases, lysosomal proteases, cathepsins and kallikreins for extracellularmatrix component degradation may play a major role in the aforementioned glioblastoma invasion mechanisms. These proteolytic networks are key players in establishing and maintaining a tumour microenvironment that promotes tumour cell survival, proliferation, and migration. Indeed, the targeted inhibition of these proteolytic enzymes has been a promisingly useful therapeutic strategy for glioblastoma management in both preclinical and clinical development. We hereby summarize current advances on the biology of the glioblastoma tumour microenvironment, with a particular emphasis on the role of proteolytic enzyme families in glioblastoma invasion and progression, as well as on their subsequent prognostic value as biomarkers and their therapeutic targeting in the era of precision medicine.

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“…Unfortunately, Cyclosporine demonstrated significant toxicity in effective doses [ 43 ]. Autophagy activation caused by ARP has a dual effect on inflammation in different cells [ 44 ]. Although, ARP 101 showed a potential effect on Sjögren’s Syndrome (autoimmune, inflammatory disease) [ 45 ].…”

Section: Resultsmentioning

confidence: 99%

In Silico Drug Repurposing in Multiple Sclerosis Using scRNA-Seq Data

Shevtsov¹,

Raevskiy

Stupnikov

et al. 2023

IJMS

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system still lacking a cure. Treatment typically focuses on slowing the progression and managing MS symptoms. Single-cell transcriptomics allows the investigation of the immune system—the key player in MS onset and development—in great detail increasing our understanding of MS mechanisms and stimulating the discovery of the targets for potential therapies. Still, de novo drug development takes decades; however, this can be reduced by drug repositioning. A promising approach is to select potential drugs based on activated or inhibited genes and pathways. In this study, we explored the public single-cell RNA data from an experiment with six patients on single-cell RNA peripheral blood mononuclear cells (PBMC) and cerebrospinal fluid cells (CSF) of patients with MS and idiopathic intracranial hypertension. We demonstrate that AIM2 inflammasome, SMAD2/3 signaling, and complement activation pathways are activated in MS in different CSF and PBMC immune cells. Using genes from top-activated pathways, we detected several promising small molecules to reverse MS immune cells’ transcriptomic signatures, including AG14361, FGIN-1-27, CA-074, ARP 101, Flunisolide, and JAK3 Inhibitor VI. Among these molecules, we also detected an FDA-approved MS drug Mitoxantrone, supporting the reliability of our approach.

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Dual functions of ARP101 in targeting membrane type‐1 matrix metalloproteinase: Impact on U87 glioblastoma cell invasion and autophagy signaling

Cited by 4 publications

References 55 publications

The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors

The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors

Extracellular proteolysis in glioblastoma progression and therapeutics

In Silico Drug Repurposing in Multiple Sclerosis Using scRNA-Seq Data

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