Piperlongumine restores the balance of autophagy and apoptosis by increasing BCL2 phosphorylation in rotenone-induced Parkinson disease models

Liu, Jia; Liu, Weijin; Lu, Yongquan; Tian, Hao; Duan, Chaojun; Lu, Lingling; Gao, Ge; Wu, Xia; Wang, Xiaomin; Yang, Hui

doi:10.1080/15548627.2017.1390636

Cited by 169 publications

(105 citation statements)

References 45 publications

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“…For instance, several studies determined that many genetic factors, such as leucine-rich repeat kinase 2 (LRRK2), glucocerebrosidase (GBA), sphingomyelin phosphodiesterase 1 (SMPD1), a-synuclein gene (SNCA), parkin RBR E3 ubiquitin protein ligase (PARK2), putative kinase 1, Parkinsonism associated deglycase (PARK7), scavenger receptor class B member 2 (SCARB2), and others, are involved in autophagy in PD (40). Accordingly, increasing B-cell lymphoma 2 phosphorylation could restore the balance of autophagy and apoptosis in rotenone-induced PD models (41). Besides, melatonin or cyclin-dependent kinase 5 knockdown could counteract the detrimental effects of MPTP-induced autophagic activity, which finally protected neuron function and prevented behavioral abnormality (42).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐124 regulates the expression of p62/p38 and promotes autophagy in the inflammatory pathogenesis of Parkinson's disease

Yao

Zhu

et al. 2019

FASEB j.

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor and nonmotor symptoms due to the selective loss of midbrain dopaminergic neurons. The evidence for a chronic inflammatory reaction mediated by microglial cells in the brain is particularly strong in PD. In our previous study, we have shown that brain‐specific microRNA‐124 (miR‐124) is significantly down‐regulated in the 1‐methy1‐4‐pheny1‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced mouse model of PD and that it can also inhibit neuroinflammation during the development of PD. However, further investigation is required to understand whether the abnormal expression of miR‐124 regulates microglial activation. In this study, we found that the expression of sequestosome 1 (p62) and phospho‐p38 mitogen‐activated protein kinases (p‐p38) showed a significant increase in LPS‐treated immortalized murine microglial cell line BV2 cells in an MPTP‐induced mouse model of PD. Knockdown of p62 could suppress the secretion of proinflammatory cytokines and p‐p38 of microglia. Besides, inhibition of p38 suppressed the secretion of proinflammatory cytokines and promoted autophagy in BV2 cells. Moreover, our study is the first to identify a unique role of miR‐124 in mediating the microglial inflammatory response by targeting p62 and p38 in PD. In the microglial culture supernatant transfer model, the knockdown of p62 in BV2 cells prevented apoptosis and death of human neuroblastoma cell lines SH‐SY5Y (SH‐SY5Y) cells following microglia activation. In addition, the exogenous delivery of miR‐124 could suppress p62 and p‐p38 expression and could also attenuate the activation of microglia in the substantia nigra par compacta of MPTP‐treated mice. Taken together, our data suggest that miR‐124 could inhibit neuroinflammation during the development of PD by targeting p62, p38, and autophagy, indicating that miR‐124 could be a potential therapeutic target for regulating the inflammatory response in PD.—Yao, L., Zhu, Z., Wu, J., Zhang, Y., Zhang, H., Sun, X., Qian, C., Wang, B., Xie, L., Zhang, S., Lu, G. MicroRNA‐124 regulates the expression of p62/p38 and promotes autophagy in the inflammatory pathogenesis of Parkinson's disease. FASEB J. 33,8648–8665 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐124 regulates the expression of p62/p38 and promotes autophagy in the inflammatory pathogenesis of Parkinson's disease

Yao

Zhu

et al. 2019

FASEB j.

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“…Autophagy is involved in cellular homeostasis, development, physiology, and abnormalities in autophagy may result in many pathophysiological conditions . LC3, Beclin 1, and p62 play key roles in the process of autophagy and have been considered specific autophagic markers . As shown in Figure A‐C, the protein levels of Beclin 1 and LC3 in the TIPE2 group were lower than those in the Mock group, whereas the expression levels of these two proteins were higher in the sh‐TIPE2 group than those in the sh‐Scb group.…”

Section: Resultsmentioning

confidence: 96%

Tumour necrosis factor‐α‐induced protein 8‐like 2 is a novel regulator of proliferation, migration, and invasion in human rectal adenocarcinoma cells

Liu

Gao

et al. 2019

J Cellular Molecular Medi

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Tumour necrosis factor‐α‐induced protein 8‐like 2 (TIPE2) is a tumour suppressor in many types of cancer. However, the mechanism of action of TIPE2 on the growth of rectal adenocarcinoma is unknown. Our results showed that the expression levels of TIPE2 in human rectal adenocarcinoma tissues were higher than those in adjacent non‐tumour tissues. Overexpression of TIPE2 reduced the proliferation, migration, and invasion of human rectal adenocarcinoma cells and down‐regulation of TIPE2 showed reverse effects. TIPE2 overexpression increased apoptosis through down‐regulating the expression levels of Wnt3a, phospho (p)‐β‐Catenin, and p‐glycogen synthase kinase‐3β in rectal adenocarcinoma cells, however, TIPE2 knockdown exhibited reverse trends. TIPE2 overexpression decreased autophagy by reducing the expression levels of p‐Smad2, p‐Smad3, and transforming growth factor‐beta (TGF‐β) in rectal adenocarcinoma cells, however, TIPE2 knockdown showed opposite effects. Furthermore, TIPE2 overexpression reduced the growth of xenografted human rectal adenocarcinoma, whereas TIPE2 knockdown promoted the growth of rectal adenocarcinoma tumours by modulating angiogenesis. In conclusion, TIPE2 could regulate the proliferation, migration, and invasion of human rectal adenocarcinoma cells through Wnt/β‐Catenin and TGF‐β/Smad2/3 signalling pathways. TIPE2 is a potential therapeutic target for the treatment of rectal adenocarcinoma.

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“…Previous study reported that the overload of mitochondria ROS resulted in the reduction of mitochondrial membrane potential (MMP) and subsequently caused the cellular apoptosis . We assessed the changes of the MMP in the spautin‐1‐treated cells with a JC‐1 probe . The cells showed a sharp MMP decline after being treated with spautin‐1 (Figure ).…”

Section: Discussionmentioning

confidence: 99%

Potent USP10/13 antagonist spautin‐1 suppresses melanoma growth via ROS‐mediated DNA damage and exhibits synergy with cisplatin

Guo

Jiangling

Liang

et al. 2020

J Cellular Molecular Medi

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Malignant melanoma is one of the most invasive tumours. However, effective therapeutic strategies are limited, and overall survival rates remain low. By utilizing transcriptomic profiling, tissue array and molecular biology, we revealed that two key ubiquitin-specific proteases (USPs), ubiquitin-specific peptidase10 (USP10) and ubiquitin-specific peptidase10 (USP13), were significantly elevated in melanoma at the mRNA and protein levels. Spautin-1 has been reported as a USP10 and USP13 antagonist, and we demonstrated that spautin-1 has potent anti-tumour effects as reflected by MTS and the colony formation assays in various melanoma cell lines without cytotoxic effects in HaCaT and JB6 cell lines. Mechanistically, we identified apoptosis and ROS-mediated DNA damage as critical mechanisms underlying the spautin-1-mediated anti-tumour effect by utilizing transcriptomics, qRT-PCR validation, flow cytometry, Western blotting and immunofluorescence staining. Importantly, by screening spautin-1 with targeted or chemotherapeutic drugs, we showed that spautin-1 exhibited synergy with cisplatin in the treatment of melanoma. Pre-clinically, we demonstrated that spautin-1 significantly attenuated tumour growth in a cell line-derived xenograft mouse model, and its anti-tumour effect was further enhanced by cotreatment with cisplatin. Taken together, our study revealed | 4325 GUO et al.

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Piperlongumine restores the balance of autophagy and apoptosis by increasing BCL2 phosphorylation in rotenone-induced Parkinson disease models

Cited by 169 publications

References 45 publications

MicroRNA‐124 regulates the expression of p62/p38 and promotes autophagy in the inflammatory pathogenesis of Parkinson's disease

MicroRNA‐124 regulates the expression of p62/p38 and promotes autophagy in the inflammatory pathogenesis of Parkinson's disease

Tumour necrosis factor‐α‐induced protein 8‐like 2 is a novel regulator of proliferation, migration, and invasion in human rectal adenocarcinoma cells

Potent USP10/13 antagonist spautin‐1 suppresses melanoma growth via ROS‐mediated DNA damage and exhibits synergy with cisplatin

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