Propofol Represses Cell Growth and Metastasis by Modulating the Circular RNA Non-SMC Condensin I Complex Subunit G/MicroRNA-200a-3p/RAB5A Axis in Glioma

Zhang, Li; Chen, Hao; Tian, Changzheng; Zheng, Daibo

doi:10.1016/j.wneu.2021.06.036

Cited by 6 publications

(2 citation statements)

References 34 publications

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“…Currently, studies on circRNAs has mainly focused on the competing endogenous RNA (ceRNA) mechanism. Hsa_-circ_0007244, an another circRNA generated from NCAPG, act as miRNA sponge on glioma proliferation and invasion [42]. However, increasing studies suggested that circRNAs can also perform biological functions by binding directly to proteins, regulating protein-protein interaction, altering the cellular localization of transcription factors, and even can be translated [10,29,43].…”

Section: Discussionmentioning

confidence: 99%

The U2AF65/circNCAPG/RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-β pathway

Jiang

et al. 2023

Cell Death Dis

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Glioma is the most aggressive and common malignant neoplasms in human brain tumors. Numerous studies have showed that glioma stem cells (GSCs)drive the malignant progression of gliomas. Recent studies have revealed that circRNAs can maintain stemness and promote malignant progression of glioma stem cells. We used bioinformatics analysis to identify circRNAs and potential RNA-binding proteins (RBPs) in glioma. qRT-PCR, western blotting, RNA FISH, RNA pull-down, RNA immunoprecipitation assay, ChIP, immunohistochemistry, and immunofluorescence methods were used to quantified the expression of circNCAPG, U2AF65, RREB1 and TGF-β1, and the underlying mechanisms between them. MTS, EDU, neurosphere formation, limiting dilution neurosphere formation and transwell assays examined the proliferation and invasive capability of GSCs, respectively. We identified a novel circRNA named circNCAPG was overexpressed and indicated the poor prognosis in glioma patients. Upregulating circNCAPG promoted the malignant progression of GSCs. RNA binding protein U2AF65 could stabilize circNCAPG by direct binding. Mechanically, circNCAPG interacted with and stabilized RREB1, as well as stimulated RREB1 nuclear translocation to activate TGF-β1 signaling pathway. Furthermore, RREB1 transcriptionally upregulated U2AF65 expression to improve the stability of circNCAPG in GSCs, which established a feedback loop involving U2AF65, circNCAPG and RREB1. Since circRNA is more stable than mRNA and can execute its function continuously, targeting circNCAPG in glioma may be a novel promising therapeutic.

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Section: Discussionmentioning

confidence: 99%

The U2AF65/circNCAPG/RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-β pathway

Jiang

et al. 2023

Cell Death Dis

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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]. However, all these studies were performed in specific established cell lines, whereas propofol effects on tumor-derived primary cultures of glioma cells and glioma stem cells and on the interaction of glioma cells and microglia cells are not yet reported.…”

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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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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Targeting miRNAs with anesthetics in cancer: Current understanding and future perspectives

Tabnak

Masrouri

Geraylow

et al. 2021

Biomedicine & Pharmacotherapy

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Propofol Represses Cell Growth and Metastasis by Modulating the Circular RNA Non-SMC Condensin I Complex Subunit G/MicroRNA-200a-3p/RAB5A Axis in Glioma

Cited by 6 publications

References 34 publications

The U2AF65/circNCAPG/RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-β pathway

The U2AF65/circNCAPG/RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-β pathway

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

Targeting miRNAs with anesthetics in cancer: Current understanding and future perspectives

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