Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway

Shi, Ligen; Lei, Jianwei; Xu, Hangzhe; Zheng, Jingwei; Wang, Yan; Peng, Yucong; Yu, Jun; Zhang, Jianmin

doi:10.18632/oncotarget.20569

Cited by 11 publications

(10 citation statements)

References 37 publications

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“…MST1 is a silk/susine protein kinase, and is an important factor in the Hippo signaling pathway. MST1 is also involved in tumor occurrence and overgrowth of cells, 23 as MST1 deficiency can cause tumor formation which is associated with apoptosis of multiple cell types. 24 Overexpression of PCMT1 has been shown to prevent apoptosis induced by Bax in neurons and COS-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway

et al. 2020

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Alzheimer’s disease (AD) is a progressive, neurodegenerative disease. Accumulating evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue (substantia nigra, blue plaque, paraventricular nucleus). In this study, we investigated the effect of neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβ25-35 significantly decreased the cell viability in time and dose dependent manner. However, Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had inhibitory effect on toxicity when fibrillation of Aβ25-35 occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβ25-35 + NSC-CDM group. sh-PCMT1 significantly reduced the PCMT1, the cell viability and inhibited the protective effect; induced apoptosis and increased the expression of p-MST1. Overexpression of PCMT1 group reversed the effect of Aβ25-35 inhibited the cell viability and Aβ25-35 induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβ25-35 to cells by increasing PCMT1, reducing MST phosphorylation.

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Section: Discussionmentioning

confidence: 99%

Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway

et al. 2020

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“…It has been reported that MST1 interacts with ROS and plays critical roles in apoptosis, autophagy, and tumor suppression (39)(40)(41)(42). Recently, studies have also demonstrated that ROS induces pyroptosis and suppresses cancer progression (43,44).…”

Section: Mst1 Suppresses Proliferation Migration and Invasion Via Rmentioning

confidence: 99%

MST1 Suppresses Pancreatic Cancer Progression via ROS-Induced Pyroptosis

Cui

Zhou

Yang

et al. 2019

Molecular Cancer Research

108

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Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease, and its incidence is increasing annually. It is critical to reveal and delineate the molecular mechanism promoting PDAC development and progression. Mammalian STE20-like kinase 1 (MST1) is a proapoptotic cytoplasmic kinase and also one of the core components of the Hippo pathway. Here, we showed that MST1 expression was decreased in PDAC, and restored expression of MST1 promoted PDAC cell death and suppressed the proliferation, migration, invasion, and cell spheroid formation of PDAC via caspase-1-induced pyroptosis. Further studies demonstrated that pyroptosis induced by MST1 was independent of the Hippo pathway, but mediated by reactive oxygen species (ROS). And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion. Collectively, our study demonstrated that MST1 suppressed the progression of PDAC cells at least partly through ROS-induced pyroptosis.Implications: In this study, we identified a new mechanism of MST1 in inhibiting PDAC development and progression and revealed that MST1 would be a potential prognostic and therapeutic target for PDAC.

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“…Sambri et al (2011) found that microRNA 15a/16-1 regulates apoptosis in hepatocellular tumor cells through PCMT1, and Liang et al (2017) showed that CGP3466B plays a neuroprotective role by regulating apoptosis through the PCMT1/Mst1 pathway in rats with traumatic brain injury. MST1 is also involved in tumor occurrence and overgrowth of cells (Perumal et al, 2017), as MST1 deficiency can cause tumor formation that is associated with apoptosis of multiple cell types (Shi et al, 2017b). Overexpression of PCMT1 has been shown to prevent apoptosis induced by Bax in neurons and COS-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SH-SY5Y cells induced by Aβ25-35

Wu¹,

Jia²,

Yang³

et al. 2022

Biocell

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A progressive neurodegenerative disease, Alzheimer's disease (AD). Studies suggest that highly expressed protein isoaspartate methyltransferase 1 (PCMT1) in brain tissue. In the current study, we explored the effects of neural stem cell-conditioned medium (NSC-CDM) on the PCMT1/MST1 pathway to alleviate Aβ 25-35 -induced damage in SH-SY5Y cells. Our data suggested that Aβ 25-35 markedly inhibited cell viability. NSC-CDM or Neural stem cell-complete medium (NSC-CPM) had a suppression effect on toxicity when treatment with Aβ 25-35 , with a greater effect observed with NSC-CDM. Aβ 25-35 + NSC-CDM group exhibited an increase in PCMT1 expression. sh-PCMT1 markedly decreased cell proliferation and suppressed the protective role of NSC-CDM through the induction of apoptosis and improved p-MST1 expression. Overexpression of PCMT1 reversed the Aβ 25-35 -induced decrease in cell proliferation and apoptosis. In summary, our findings suggest that NSC-CDM corrects the Aβ 25-35induced damage to cells by improving PCMT1 expressions, which in turn reduces phosphorylation of MST1.

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Hydrogen sulfide ameliorates subarachnoid hemorrhage-induced neuronal apoptosis via the ROS-MST1 pathway

Cited by 11 publications

References 37 publications

Neural stem cell conditioned medium alleviates Aβ<sub>25-35</sub> damage to SH-SY5Y cells through the PCMT1/MST1 pathway

Neural stem cell conditioned medium alleviates Aβ<sub>25-35</sub> damage to SH-SY5Y cells through the PCMT1/MST1 pathway

MST1 Suppresses Pancreatic Cancer Progression via ROS-Induced Pyroptosis

Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SH-SY5Y cells induced by Aβ25-35

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