Signal Transducer and Activator of Transcription 3 (STAT3) Degradation by Proteasome Controls a Developmental Switch in Neurotrophin Dependence

Murase, Sachiko

doi:10.1074/jbc.m113.470583

Cited by 22 publications

(14 citation statements)

References 58 publications

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“…Neurons that survive during this period become resistant to neurotrophin deprivation. STAT3 has been proven to be a key regulator of neural survival during this stage [15]. Notably, this phase roughly corresponds to the time window of neural vulnerability to isoflurane [22].…”

Section: Discussionmentioning

confidence: 97%

“…The activity of calcineurin was determined in the freshly obtained frontal cortex using a colorimetric calcineurin cellular activity assay kit (Calbiochem, Germany) as described previously [15]. Calcineurin is not the only phosphatase in the brain, and it requires calcium for its activity; it has been proven to be completely inhibited by ethylene glycol tetraacetic acid (EGTA).…”

Section: Calcineurin Activity Assaysmentioning

confidence: 99%

“…Calcineurin has been shown to specifically promote STAT3 degradation in the brain and in primary neurons [15]; thus, a calcineurin-specific inhibitor, FK506, was introduced in the next study. Our data showed that pretreatment with FK506 attenuated isoflurane-induced STAT3 degradation (P = 0.028) and caspase-3 cleavage (P = 0.025) in the frontal cortex of neonatal mice ( Fig.…”

Section: Calcineurin Was Involved In Isoflurane-induced Stat3 Degradamentioning

confidence: 99%

“…STAT3 serves as a key molecule downstream of neurotrophin signaling and enables mature neurons to achieve resistance against neurotrophin deprivation. Overexpression of STAT3 in immature neurons has been shown to attenuate death caused by neurotrophin insufficiency [15,16]. The present research used a combination of in-vitro and in-vivo studies to determine whether isoflurane would target STAT3 to deliver its neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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STAT3 degradation mediated by calcineurin involved in the neurotoxicity of isoflurane

Yang

Song²,

Min³

et al. 2016

NeuroReport

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Isoflurane, a commonly used volatile anesthetic, causes widespread neuronal apoptosis in the developing brain of rodents. Signal transducer and activator of transcription-3 (STAT3) signaling is crucial for cell survival during the neural network establishment period. The aim of this study was to determine whether isoflurane would target STAT3 to deliver its neurotoxicity. Mice at postnatal day 7 and primary cortical neurons cultured for 5 days were treated with isoflurane. Our data showed that isoflurane exposure downregulated the STAT3 survival pathway in the brain of mice and in primary neurons, whereas the mRNA levels of STAT3 remained unchanged after isoflurane exposure. We found that inhibiting the activity of calcineurin, which specifically promotes STAT3 degradation, alleviated isoflurane-induced neural apoptosis. Further studies showed that isoflurane increased calcineurin activity and that the inositol 1,4,5-trisphosphate-sensitive Ca(2+) channel was involved in these isoflurane-induced molecular cascades. These findings suggest that isoflurane-induced neurotoxicity may stem from STAT3 degradation, partially through the activation of calcineurin.

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Section: Discussionmentioning

confidence: 97%

Section: Calcineurin Activity Assaysmentioning

confidence: 99%

Section: Calcineurin Was Involved In Isoflurane-induced Stat3 Degradamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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STAT3 degradation mediated by calcineurin involved in the neurotoxicity of isoflurane

Yang

Song²,

Min³

et al. 2016

NeuroReport

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“…Neurotrophins are a family of trophic factors, which are involved in differentiation and survival of neural cells (23,24). This family consists of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), and neurotrophin 4 (NT-4).…”

Section: Discussionmentioning

confidence: 99%

mRNA and microRNA expression profiles of radioresistant NCI-H520 non-small cell lung cancer cells

Guo

Xie

Zhao

et al. 2015

Molecular Medicine Reports

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To elucidate the mechanism of radioresistance in non-small cell lung cancer (NSCLC) cells and to identify key molecules conferring radioresistance, the radioresistant subclone NCI-H520/R, derived from the NCI-H520 NSCLC cell line, was established with eight rounds of sublethal irradiation. The radioresistant features were subsequently assessed using a clonogenic assay, analysis of apoptosis and an MTT assay, the gene expression levels were examined using an Agilent Whole Human Genome 4×44 k Oligo microarray and Agilent Human miRCURY™ LNA array, and confirmed by reverse transcription-quantitative polymerase chain reaction. Pathway analysis and Gene Ontology (GO) analysis were performed to determine the biological functions of the subset of differentially expressed genes. miRNA-mRNA correlation analysis between the expression levels of each miRNA and all its predicted target genes was performed to further understand the radioresistance in the NCI-H520 cells. Following eight rounds of sublethal irradiation, a total of 2,862 mRNAs were significantly differentially expressed in the NCI-H520/R cells, including 893 upregulated genes and 1,969 downregulated genes. A total of 162 upregulated miRNAs and 274 downregulated miRNAs were significantly deregulated in the NCI-H520/R cells. Multiple core regulatory processes and signaling pathways were identified as being of likely relevance to radioresistance in NCI-H520/R cells, including the mitogen-activated protein kinase signaling pathway and neurotrophin signaling pathway. The expression of genes associated with radioresistance reflects the complex biological processes involved in clinical cancer cell eradication and requires further investigation for future enhancement of therapy.

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Phosphorylation of STAT3 at Tyr705 contributes to TFEB-mediated autophagy-lysosomal pathway dysfunction and leads to ischemic injury in rats

Liu

Che

et al. 2023

Cell. Mol. Life Sci.

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Signal Transducer and Activator of Transcription 3 (STAT3) Degradation by Proteasome Controls a Developmental Switch in Neurotrophin Dependence

Cited by 22 publications

References 58 publications

STAT3 degradation mediated by calcineurin involved in the neurotoxicity of isoflurane

STAT3 degradation mediated by calcineurin involved in the neurotoxicity of isoflurane

mRNA and microRNA expression profiles of radioresistant NCI-H520 non-small cell lung cancer cells

Phosphorylation of STAT3 at Tyr705 contributes to TFEB-mediated autophagy-lysosomal pathway dysfunction and leads to ischemic injury in rats

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