Propofol-induced neurotoxicity in hESCs involved in activation of miR-206/PUMA signal pathway

Yu, Li; Jia, Changxin; Zhang, Dianlong; Ni, Guangzhen; Miao, Xiangshui; Tu, Ruirong

doi:10.3233/cbm-170167

Cited by 15 publications

(16 citation statements)

References 31 publications

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“…In fact, several previous studies have implicated the functions of propofol on miRNA expression. For example, miR‐372, miR‐195, miR‐1284, miR‐206, miR‐9 and miR‐21 were all stated to be affected by propofol to control cell growth, migration and invasion . Additionally, here ADAM8 was identified to directly target to miR‐328.…”

Section: Discussionmentioning

confidence: 99%

“…For example, miR-372, miR-195, miR-1284, miR-206, miR-9 and miR-21 were all stated to be affected by propofol to control cell growth, migration and invasion. [14][15][16][17][18][19] Additionally, here ADAM8 was identified to directly target to miR-328. Our results implicate that propofol exerts an inhibitory effect on pancreatic cancer cell growth, migration and invasion by enhancing miR-328 which targets ADAM8.…”

Section: Discussionmentioning

confidence: 99%

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Propofol inhibits pancreatic cancer proliferation and metastasis by up‐regulating miR‐328 and down‐regulating ADAM8

Gao

Zhang

2019

Basic Clin Pharma Tox

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Propofol is commonly used for anaesthesia during surgery, and accumulating evidence has demonstrated that propofol is associated with tumour suppression. For example, propofol down‐regulates the expression of vascular endothelial growth factor to inhibit pancreatic cancer malignancy. However, deeper insights into its underlying mechanism are needed. In this study, we treated pancreatic cell lines Panc1 and Bxpc3 with or without propofol. Cell proliferation, migration and invasion were evaluated using 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and transwell assays. Real‐time polymerase chain reaction was used to measure RNA expression levels. Luciferase assay was performed to determine the transcriptional activity of microRNAs (miRNAs). We found that propofol significantly reduced the proliferation, migration and invasion of pancreatic cancer cells compared to untreated cells. By testing the changes in miRNAs after propofol treatment, propofol was shown to strikingly enhance the expression of miR‐328. Luciferase assays demonstrated that propofol repressed the transcriptional activity of miR‐328, while a disintegrin and metalloproteinase 8 (ADAM8) was a direct target of miR‐328. Knockdown of miR‐328 or ADAM8 led to significantly decreased cell growth and viability. Our results implicate that propofol inhibits pancreatic cancer growth and metastasis by enhancing miR‐328 which targets ADAM8.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Propofol inhibits pancreatic cancer proliferation and metastasis by up‐regulating miR‐328 and down‐regulating ADAM8

Gao

Zhang

2019

Basic Clin Pharma Tox

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“…[17][18][19] Further, miR-206 knockdown was shown to protect human embryonic stem cells (hESCs) against propofol-induced cell apoptosis, thereby inhibiting neurotoxicity. 20 Rho-associated coiled coil-containing protein kinase 1 (ROCK1) is a protein serine/threonine kinase and a major regulator of the actomyosin cytoskeleton, thereby governing various cellular processes, including cell division, adhesion, contraction, migration, apoptosis, and proliferation. 21 Accumulating studies have indicated that ROCK1 plays crucial roles in cancer development by modulating diverse vital cellular biological processes related to malignancy.…”

Section: Introductionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear. Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay. Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells. Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.

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“…Total RNA was isolated from hESC-derived neurons with TRIzol reagent (Invitrogen, Shanghai, China) and reverse-transcribed into cDNA using oligo (dT) 15 and ReverTra Ace reverse transcriptase (Toyobo, Osaka, Japan). NanoDrop 2000 (Thermo Scientific, Wilmington, DE, USA) was used to quantify amounts of mRNA.…”

Section: Rna Extraction and Real-time Qrt-pcrmentioning

confidence: 99%

“…Li et al have reported that propofol induces cell apoptosis in hESC-derived neurons via activation of the miR-206/PUMA signal pathway [14]. And Jiang et al have reported that propofol inhibits hESCs neurogenesis through a mechanism involving the miR-141-3p/IGF2BP2 axis [15].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-665 mediates propofol-induced cell apoptosis in human stem cell-derived neurons

et al. 2019

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We aimed to evaluate the neurotoxicity and mechanisms of anesthetics propofol in hESC-derived neurons. Cell apoptosis in hESC-derived neurons' exposure to 4, 10 and 20 μg/mL propofol for 6 h was assessed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate in situ nick end labeling (TUNEL) staining and microRNA-665 (miR-665) expression was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-665 was overexpressed and knocked down using a miR-665 mimic and anti-665 transfection, respectively. The results showed that hESCs exposed to propofol showed a dose-dependent cell apoptosis, followed by the upregulation of miR-665 expression. Overexpression of miR-665 increased propofol-induced apoptosis in hESC cells. And targeting miR-665 decreased propofol-induced cell apoptosis in hESC cells. These data suggest that propofol induces cell death in hESC-derived neurons and the propofol-induced cell apoptosis may occur via miR-665-dependent mechanism.

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Propofol-induced neurotoxicity in hESCs involved in activation of miR-206/PUMA signal pathway

Abstract: Propofol induce s cell death in hESC-derived neurons via activation of miR-206/PUMA signal pathway.

Cited by 15 publications

References 31 publications

Propofol inhibits pancreatic cancer proliferation and metastasis by up‐regulating miR‐328 and down‐regulating ADAM8

Propofol inhibits pancreatic cancer proliferation and metastasis by up‐regulating miR‐328 and down‐regulating ADAM8

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

MicroRNA-665 mediates propofol-induced cell apoptosis in human stem cell-derived neurons

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