In Vitro Effects of Propofol on Cytotoxic, Apoptotic and PI3K-Akt Signaling Pathway
Genes on Brain Cancer Cells

Edgünlü, Tuba Gökdoğan; Avcı, Çığır Biray; Özateş, Neslihan Pınar; Bağca, Bakiye Göker; Çelik, Sevim; Bölük, Aydın; Uğur, Bakiye

doi:10.2174/1871520621666210708094328

Cited by 5 publications

(4 citation statements)

References 29 publications

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“…More consistent effects have been reported on in vitro and animal studies, which demonstrated anti-tumor effects of propofol in a variety of solid tumors [21,22,55], further supporting these observations. Similarly, anti-tumor effects of propofol were reported on different glioma cell lines both in vitro and in vivo, mostly demonstrating changes in cell proliferation, migration [56,57], and inhibition of tumor growth [57,58].…”

Section: Discussionsupporting

confidence: 81%

“…The choice of general anesthetic for tumor surgical resection has been recently reported to impact tumor growth, metastasis, and recurrence, as well as prognosis of patients with solid tumors [18,19,22]. Propofol, one of the most commonly used anesthetics during surgery, has been mainly associated with anti-tumor effects, while few studies report an opposite effect [19,22,55]. Retrospective epidemiological studies demonstrate that the use of propofol during resection is associated with a better prognosis than other general anesthetics in patients with different solid tumors [18,20].…”

Section: Discussionmentioning

confidence: 99%

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Propofol Inhibits Glioma Stem Cell Growth and Migration and Their Interaction with Microglia via BDNF-AS and Extracellular Vesicles

Nizar,

Cazacu,

Xiang

et al. 2023

Cells

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Glioblastoma (GBM) is the most common and aggressive primary brain tumor. GBM contains a small subpopulation of glioma stem cells (GSCs) that are implicated in treatment resistance, tumor infiltration, and recurrence, and are thereby considered important therapeutic targets. Recent clinical studies have suggested that the choice of general anesthetic (GA), particularly propofol, during tumor resection, affects subsequent tumor response to treatments and patient prognosis. In this study, we investigated the molecular mechanisms underlying propofol’s anti-tumor effects on GSCs and their interaction with microglia cells. Propofol exerted a dose-dependent inhibitory effect on the self-renewal, expression of mesenchymal markers, and migration of GSCs and sensitized them to both temozolomide (TMZ) and radiation. At higher concentrations, propofol induced a large degree of cell death, as demonstrated using microfluid chip technology. Propofol increased the expression of the lncRNA BDNF-AS, which acts as a tumor suppressor in GBM, and silencing of this lncRNA partially abrogated propofol’s effects. Propofol also inhibited the pro-tumorigenic GSC-microglia crosstalk via extracellular vesicles (EVs) and delivery of BDNF-AS. In conclusion, propofol exerted anti-tumor effects on GSCs, sensitized these cells to radiation and TMZ, and inhibited their pro-tumorigenic interactions with microglia via transfer of BDNF-AS by EVs.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Propofol Inhibits Glioma Stem Cell Growth and Migration and Their Interaction with Microglia via BDNF-AS and Extracellular Vesicles

Nizar,

Cazacu,

Xiang

et al. 2023

Cells

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“…In addition to its effect on reducing pain, propofol has potential antitumor activity. Various reports have shown that propofol induces cytotoxicity in different cancer cells, including glioma [366][367][368]. Shu-Shong et al reported that it generates cytotoxicity in 8401 human GB cells through ROSassociated apoptosis in a concentration-dependent manner that induces cell cycle G2/M arrest and caspase activation [369].…”

Section: Propofolmentioning

confidence: 99%

Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells

Trejo-Solís,

Castillo-Rodríguez,

Serrano-García

et al. 2024

Metabolites

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The metabolic reprogramming that promotes tumorigenesis in glioblastoma is induced by dynamic alterations in the hypoxic tumor microenvironment, as well as in transcriptional and signaling networks, which result in changes in global genetic expression. The signaling pathways PI3K/AKT/mTOR and RAS/RAF/MEK/ERK stimulate cell metabolism, either directly or indirectly, by modulating the transcriptional factors p53, HIF1, and c-Myc. The overexpression of HIF1 and c-Myc, master regulators of cellular metabolism, is a key contributor to the synthesis of bioenergetic molecules that mediate glioma cell transformation, proliferation, survival, migration, and invasion by modifying the transcription levels of key gene groups involved in metabolism. Meanwhile, the tumor-suppressing protein p53, which negatively regulates HIF1 and c-Myc, is often lost in glioblastoma. Alterations in this triad of transcriptional factors induce a metabolic shift in glioma cells that allows them to adapt and survive changes such as mutations, hypoxia, acidosis, the presence of reactive oxygen species, and nutrient deprivation, by modulating the activity and expression of signaling molecules, enzymes, metabolites, transporters, and regulators involved in glycolysis and glutamine metabolism, the pentose phosphate cycle, the tricarboxylic acid cycle, and oxidative phosphorylation, as well as the synthesis and degradation of fatty acids and nucleic acids. This review summarizes our current knowledge on the role of HIF1, c-Myc, and p53 in the genic regulatory network for metabolism in glioma cells, as well as potential therapeutic inhibitors of these factors.

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“…In addition, some anesthetic drugs such as propofol, dexmedetomidine and thiopental sodium may affect the malignant phenotype of tumor cells in some way [ 8 , 9 ]. These anesthetics are considered potential tumor suppressors or facilitators, but their effects in glioma remain to be revealed [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Co-expression prognostic-related genes signature base on propofol and sevoflurane anesthesia predict prognosis and immunotherapy response in glioblastoma

Hou

Luo

et al. 2023

Annals of Medicine

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Objectives Anesthetic drugs had been reported may impact the bio-behavior of the tumor. Propofol and sevoflurane are common anesthetics in the operation for glioblastoma (GBM). This study aims to establish a co-expression prognostic-related genes signature base on propofol and sevoflurane anesthesia to predict prognosis and immunotherapy response in GBM. Method GPM tissues with different anesthetics gene expression profiles (GSE179004) were obtained from the Gene Expression Omnibus (GEO) database. Core modules and central genes associated with propofol and sevoflurane anesthesia were identified by weighted gene coexpression network analysis (WGCNA) and establish a risk score prognostic model. Immune cell signature analysis in TCGA datasets was predicted via CIBERSORT. At last, serum methylation level of O6-methylguanine-DNA methyltransferase (MGMT) promoter was detected in GPM patient in different time during perioperative period. Results The burlywood1 group screened was significantly associated with sevoflurane-treated GBM tissue. 22 independent prognostic differential genes were construct a prognostic-related genes risk score in GBM, and showed good predictive ability. The risk score was strongly correlated with the age of the patients, but not with the sex of the patients. In addition, the differential responses to immunotherapy in high and low risk groups were analyzed, indicating that sevoflurane signature genes were consistent in the classification of gliomas. High-risk patients have high T-cell damage score and are less sensitive to immunotherapy. At last, serum methylation level of MGMT promoter was decreased in GBM patients during propofol and sevoflurane anesthesia. Conclusions Propofol and sevoflurane anesthesia associated impact on the gene expression of GBM, included the methylation level of MGMT promoter. Propofol and sevoflurane anesthesia-based risk score prognostic model, which has good prognostic power and is an independent prognostic factor in GBM patients. Therefore, this model can be used as a new biomarker for judging the prognosis of GBM patients. KEY MESSAGES Propofol and sevoflurane anesthesia-based risk score prognostic model has good prognostic power and is an independent prognostic factor in GBM patients. High Propofol and sevoflurane anesthesia-based risk score GBM patients have high T-cell damage scores and are less sensitive to immunotherapy. Serum methylation level of MGMT promoter decrease during propofol and sevoflurane anesthesia in GBM patients.

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In Vitro Effects of Propofol on Cytotoxic, Apoptotic and PI3K-Akt Signaling Pathway Genes on Brain Cancer Cells

Cited by 5 publications

References 29 publications

Propofol Inhibits Glioma Stem Cell Growth and Migration and Their Interaction with Microglia via BDNF-AS and Extracellular Vesicles

Propofol Inhibits Glioma Stem Cell Growth and Migration and Their Interaction with Microglia via BDNF-AS and Extracellular Vesicles

Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells

Co-expression prognostic-related genes signature base on propofol and sevoflurane anesthesia predict prognosis and immunotherapy response in glioblastoma

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