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Article ; Online: c-Jun phosphorylated by JNK is required for protecting Gli2 from proteasomal-ubiquitin degradation by PGE2-JNK signaling axis.

Yang, Jun / Wang, Juan / Zhang, Yu / Huang, Wenjing / Zhang, Shaoqing / Yin, Peihao / Tan, Wenfu

Biochimica et biophysica acta. Molecular cell research

2022 Volume 1870, Issue 3, Page(s) 119418

Abstract: ... signaling pathway. In this study, we showed that c-Jun, a classic substrate of JNK, increased Gli2 protein stability ... after phosphorylated by PGE2. Suppressing the function of c-Jun or JNK indicated that c-Jun prevents ... of Gli2 was detected in colorectal cancer cells treated with PGE2 while suppression of c-Jun restored ...

Abstract	Hedgehog (Hh) signaling pathway includes canonical and non-canonical activation manners. In colorectal cancer, we have previously shown that PGE2-JNK could initiate non-canonical activation of the Hh signaling pathway. In this study, we showed that c-Jun, a classic substrate of JNK, increased Gli2 protein stability after phosphorylated by PGE2. Suppressing the function of c-Jun or JNK indicated that c-Jun prevents Gli2 from protease degradation caused by PGE2-JNK. Moreoer, we revealed that less ubiquitination of Gli2 was detected in colorectal cancer cells treated with PGE2 while suppression of c-Jun restored the ubiquitination of Gli2. In addition, we observed that suppression of c-Jun significantly decreased Gli2 expression no matter when Gli2 remained in phosphorylation or non-phosphorylation state. These phenomena were recapitulated, when the endpoint of Gli2 expression was replaced by Gli2 ubiquitination. Furthermore, we demonstrated that restricting c-Jun function ablated the PGE2-provoked Hh activity and proliferation of colorectal cancer cells. These results elucidated that the evasion of Gli2 with phosphorylation from proteasomal-ubiquitin degradation needed the cooperation of phosphorylated c-Jun by kinase JNK, which contributed to promoting Hh activation and the proliferation of colorectal cancer cells. This study provides a theoretical foundation to target PGE2 downstream for the prevention and treatment of colorectal cancer.
MeSH term(s)	Humans ; Colorectal Neoplasms ; Dinoprostone ; Hedgehog Proteins/metabolism ; Kruppel-Like Transcription Factors/metabolism ; Nuclear Proteins ; Ubiquitin/metabolism ; Zinc Finger Protein Gli2 ; Proto-Oncogene Proteins c-jun/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Dinoprostone (K7Q1JQR04M) ; GLI2 protein, human ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nuclear Proteins ; Ubiquitin ; Zinc Finger Protein Gli2 ; Proto-Oncogene Proteins c-jun ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-12-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2022.119418
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Article ; Online: Corrigendum to "Hemoporfin-mediated photodynamic therapy for the treatment of port-wine stain: A multicenter, retrospective study" [Photodiagnosis Photodyn Ther. 2023 Jun;42:103545].

Zhang, Xiaofeng / Yuan, Chen / Xiao, Xuemin / Yin, Rui / Lei, Hongzhao / Li, Yan / Zheng, Shumao / Wen, Sijian / Li, Dongsheng / Wang, Xuejun / Lu, Zhong / Zhang, Yunfeng / Zeng, Weihui / He, Sijin / Li, Yuzhen / Jian, Dan / Yang, Jun / Zhong, Hua / Han, Dawei /

Chen, Xiaoying / Zhou, Junfeng / Cai, Yantao / Peng, Xi / Li, Zhiming / Liu, Xueying / Lin, Tong / Zhang, Ruzhi / Li, Guang / Zhuang, Yin / Liu, Ling / Yan, Yan / Wang, Baoxi

Photodiagnosis and photodynamic therapy

2023 Volume 45, Page(s) 103931

Language	English
Publishing date	2023-12-26
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2149918-4
ISSN	1873-1597 ; 1572-1000
ISSN (online)	1873-1597
ISSN	1572-1000
DOI	10.1016/j.pdpdt.2023.103931
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Article ; Online: Shengjihuayu formula ameliorates the oxidative injury in human keratinocytes via blocking JNK/c-Jun/MMPs signaling pathway.

Sun, Lu / Yin, Hao / Li, Yu-Ting / Qiao, Yun-Xiao / Wang, Jie / He, Qing-Yi / Xiao, Zhen-Wei / Kuai, Le / Xiang, Yan-Wei

Journal of ethnopharmacology

2024 Volume 326, Page(s) 117938

Abstract: ... PRDX1, HSP90AA1, HSP90AB1, HSPA8, and TNF-α. Western blot revealed the presence of the JNK/c-Jun/MMPs ...

Abstract	Ethnopharmacological relevance: The reactive oxygen species (ROS) surge in the chronic wound tissue of diabetic ulcers (DUs) aggravates the inflammatory response. The oxidative stress state during inflammation will exacerbate inflammation and cause tissue damage, resulting in prolonged wound healing. Shengjihuayu Formula (SJHYF) is a renowned Chinese medicine prescription for treating chronic wounds in diabetic ulcers. Growing clinical evidence has demonstrated that SJHYF exhibits superior therapeutic efficacy and has a favorable safety profile. However, the underlying mechanisms by which SJHYF ameliorates oxidative damage under pathological conditions of DUs remain unclear. Objective: To investigate the cytoprotective properties of SJHYF on hydrogen peroxide (H Methods: HaCaT cells were incubated with H Results: The application of SJHY at a concentration of 0.25 mg/mL promoted cell proliferation, cell migration, and reduced ROS production. In addition, SJHYF was detected to have a total of 93 active compounds, including key components such as Galloyl-beta-D-glucose, Danshensu, Procyanidin B2, Catechin, and Alkannin. The RNA-seq analysis identified several core targets namely KRT17, TGM1, JUNB, PRDX5, TXNIP, PRDX1, HSP90AA1, HSP90AB1, HSPA8, and TNF-α. Western blot revealed the presence of the JNK/c-Jun/MMPs pathway and its related transcription factors. Conclusion: SJHYF displays significant protective effects on H
MeSH term(s)	Humans ; Reactive Oxygen Species/metabolism ; Hydrogen Peroxide/metabolism ; Ulcer ; Oxidative Stress ; Keratinocytes ; MAP Kinase Signaling System ; Inflammation/metabolism ; Diabetes Mellitus/metabolism ; Apoptosis ; Glucose
Chemical Substances	Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; beta-d-glucose ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2024-02-22
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2024.117938
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Article ; Online: https://elsevier.proofcentral.com/en-us/landing-page.html?token=baf280639f2773e07701834b1c13daInhibition of spermatogenesis by hypoxia is mediated by V-ATPase via the JNK/c-Jun pathway in mice.

Yin, Jun / He, Wenjuan / Zhang, Mengjie / He, Wei / Zhang, Gang / Ni, Bing

Reproductive biology

2023 Volume 23, Issue 2, Page(s) 100761

Abstract: Spermatocyte apoptosis is the primary cause of a poor outcome after hypoxia-triggered spermatogenesis reduction (HSR). Vacuolar ... ...

Abstract	Spermatocyte apoptosis is the primary cause of a poor outcome after hypoxia-triggered spermatogenesis reduction (HSR). Vacuolar H
MeSH term(s)	Male ; Mice ; Animals ; Signal Transduction ; Adenosine Triphosphatases/pharmacology ; Spermatogenesis ; MAP Kinase Signaling System ; Apoptosis ; Hypoxia
Chemical Substances	Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2023-04-04
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2189316-0
ISSN	2300-732X ; 1642-431X
ISSN (online)	2300-732X
ISSN	1642-431X
DOI	10.1016/j.repbio.2023.100761
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Article ; Online: Salidroside ameliorated the pulmonary inflammation induced by cigarette smoke via mitigating M1 macrophage polarization by JNK/c-Jun.

Feng, Haoshen / Zhang, Dan / Yin, Yan / Kang, Jian / Zheng, Rui

Phytotherapy research : PTR

2023 Volume 37, Issue 9, Page(s) 4251–4264

Abstract: ... salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 ... c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via ... inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs ...

Abstract	Pulmonary inflammation induced by cigarette smoke (CS) promoted the development of chronic obstructive pulmonary disease (COPD), and macrophage polarization caused by CS modulated inflammatory response. Previous studies indicated that salidroside exerted therapeutic effects in COPD, but the anti-inflammatory mechanisms were not clear. This study aimed to explore the effects and mechanisms of salidroside on macrophage polarization induced by CS. Wistar rats received passively CS exposure and were treated intraperitoneally with salidroside at a low, medium or high dose. Lung tissues were stained with hematoxylin-eosin. Emphysema and inflammatory scores were evaluated by histomorphology. Lung function, cytokines, and cell differential counts in BALF were detected. The macrophage polarization was determined by immunohistochemistry in lung tissues. Alveolar macrophages (AMs) were isolated and treated with cigarette smoke extract (CSE), salidroside or inhibitors of relative pathways. The polarization status was determined by qPCR, and the protein level was detected by Western blotting. CS exposure induced emphysema and lung function deterioration. The inflammatory scores, cytokines level and neutrophils counts were elevated after CS exposure. Salidroside treatment partly ameliorated above abnormal. CS exposure activated M1 and M2 polarization of AMs in vivo and in vitro, and salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 polarization of AMs was inhibited by the inhibitors of JNK and AP-1. Salidroside treatment deactivated the JNK/c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs induced by CS, and the process might be mediated by the deactivation of JNK/c-Jun.
MeSH term(s)	Rats ; Animals ; Cigarette Smoking ; Rats, Wistar ; Lung ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pneumonia ; Pulmonary Emphysema/chemically induced ; Pulmonary Emphysema/metabolism ; Macrophages/metabolism ; Cytokines/metabolism ; Emphysema/metabolism
Chemical Substances	rhodioloside (M983H6N1S9) ; Cytokines
Language	English
Publishing date	2023-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.7905
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Article ; Online: Inhibition of c-Jun in AgRP neurons increases stress-induced anxiety and colitis susceptibility.

Jiao, Fuxin / Hu, Xiaoming / Yin, Hanrui / Yuan, Feixiang / Zhou, Ziheng / Wu, Wei / Chen, Shanghai / Liu, Zhanju / Guo, Feifan

Communications biology

2023 Volume 6, Issue 1, Page(s) 50

Abstract: ... respectively. Furthermore, CRS inhibits AgRP neuronal activity by suppressing the expression of c-Jun. Moreover ... overexpression of c-Jun in these neurons protects against the CRS-induced effects, and knockdown of c-Jun in AgRP ... neurons (c-Jun ...

Abstract	Psychiatric disorders, such as anxiety, are associated with inflammatory bowel disease (IBD), however, the neural mechanisms regulating this comorbidity are unknown. Here, we show that hypothalamic agouti-related protein (AgRP) neuronal activity is suppressed under chronic restraint stress (CRS), a condition known to increase anxiety and colitis susceptibility. Consistently, chemogenic activation or inhibition of AgRP neurons reverses or mimics CRS-induced increase of anxiety-like behaviors and colitis susceptibility, respectively. Furthermore, CRS inhibits AgRP neuronal activity by suppressing the expression of c-Jun. Moreover, overexpression of c-Jun in these neurons protects against the CRS-induced effects, and knockdown of c-Jun in AgRP neurons (c-Jun
MeSH term(s)	Mice ; Animals ; Agouti-Related Protein/genetics ; Agouti-Related Protein/metabolism ; Hypothalamus/metabolism ; Anxiety/etiology ; Neurons/physiology ; Colitis/genetics ; Colitis/metabolism
Chemical Substances	Agouti-Related Protein
Language	English
Publishing date	2023-01-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-04425-w
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Article ; Online: SENP3-mediated deSUMOylation of c-Jun facilitates microglia-induced neuroinflammation after cerebral ischemia and reperfusion injury.

Xia, Qian / Mao, Meng / Zhan, Gaofeng / Luo, Zhenzhao / Zhao, Yin / Li, Xing

iScience

2023 Volume 26, Issue 6, Page(s) 106953

Abstract: ... in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun ... by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 ... expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic ...

Abstract	Recent evidences have implicated that SENP3 is a deSUMOylase which possesses neuronal damage effects in cerebral ischemia. However, its role in microglia remains poorly understood. Here, we found that SENP3 was upregulated in the peri-infarct areas of mice following ischemic stroke. Furthermore, knockdown of SENP3 significantly inhibits the expression of proinflammatory cytokines and chemokines in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun, which activated its transcriptional activity, ultimately followed by the activation of MAPK/AP-1 signaling pathway. In addition, microglia-specific SENP3 knockdown alleviated ischemia-induced neuronal damage, and markedly diminished infract volume, ameliorated sensorimotor and cognitive function in animals subjected to ischemic stroke. These results indicated SENP3 functions as a novel regulator of microglia-induced neuroinflammation by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic stroke.
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106953
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Article ; Online: Low-Dose Trans-Resveratrol Ameliorates Diabetes-Induced Retinal Ganglion Cell Degeneration via TyrRS/c-Jun Pathway.

Xiao, Ke / Ma, Xiao-Hong / Zhong, Zheng / Zhao, Yin / Chen, Xu-Hui / Sun, Xu-Fang

Investigative ophthalmology & visual science

2023 Volume 64, Issue 7, Page(s) 2

Abstract: ... on the binding of TyrRS to the transcription factor c-Jun and the binding of c-Jun to pro-apoptotic genes were ... and HG-treated N2a cells. Trans-RSV promoted TyrRS binding to c-Jun, inhibited the phosphorylation ... of Ser-63 of c-Jun, and downregulated pro-apoptotic gene transcription.: Conclusions: Low-dose trans ...

Abstract	Purpose: The purpose of this study was to investigate the protective effect of low-dose trans-resveratrol (trans-RSV) on diabetes-induced retinal ganglion cell (RGC) degeneration and its possible mechanism. Methods: A streptozotocin-induced diabetic mouse model was established and treated with or without trans-RSV intragastric administration (10 mg/kg body weight/day) for 12 weeks. Oscillatory potentials (Ops) of the dark-adapted electroretinogram (ERG) were recorded. The number of RGCs was detected by Tuj1 and TUNEL staining. The apoptosis markers in the retina were analyzed by Western blot. The cross sections of optic nerves were observed by transmission electron microscopy. In addition, mouse neuroblastoma N2a cells were injured by high-glucose (HG) treatment. Cell viability and apoptosis were measured with or without low-dose trans-RSV treatment. The intracellular localization of tyrosyl transfer-RNA synthetase (TyrRS) was observed in both mouse retinas and N2a cells. The effects of low-dose trans-RSV on the binding of TyrRS to the transcription factor c-Jun and the binding of c-Jun to pro-apoptotic genes were analyzed by co-IP and ChIP assays in HEK 293 cells. Results: Trans-RSV relieved electrophysiological injury of retinas and inhibited RGC apoptosis in diabetic mice. It also protected N2a cells from HG-induced apoptosis. Additionally, it promoted TyrRS nuclear translocation in both diabetic mouse retinas and HG-treated N2a cells. Trans-RSV promoted TyrRS binding to c-Jun, inhibited the phosphorylation of Ser-63 of c-Jun, and downregulated pro-apoptotic gene transcription. Conclusions: Low-dose trans-RSV can ameliorate diabetes-induced RGC degeneration via the TyrRS/c-Jun pathway. It can promote TyrRS nuclear translocation and bind to c-Jun, downregulating c-Jun phosphorylation and downstream pro-apoptotic genes.
MeSH term(s)	Mice ; Humans ; Animals ; Retinal Ganglion Cells/metabolism ; Resveratrol/pharmacology ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; HEK293 Cells ; Retina/metabolism ; Apoptosis
Chemical Substances	Resveratrol (Q369O8926L)
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.64.7.2
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Article ; Online: Identification of the c-Jun/H19/miR-19/JNK1 cascade during hepatic stellate cell activation.

Sun, Ying / Liu, Chunyu / Guo, Xu / Zhao, Jiayu / Xiao, Anqi / Yin, Kai / Liu, Ming / Sun, Xinlei / Chen, Xi / Liu, Minghui

Clinical and translational medicine

2023 Volume 13, Issue 3, Page(s) e1106

MeSH term(s)	Hepatic Stellate Cells ; MicroRNAs/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2697013-2
ISSN	2001-1326 ; 2001-1326
ISSN (online)	2001-1326
ISSN	2001-1326
DOI	10.1002/ctm2.1106
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Article ; Online: B4GALNT1 promotes progression and metastasis in lung adenocarcinoma through JNK/c-Jun/Slug pathway.

Jiang, Tian / Wu, Hao / Lin, Miao / Yin, Jun / Tan, Lijie / Ruan, Yuanyuan / Feng, Mingxiang

Carcinogenesis

2020 Volume 42, Issue 4, Page(s) 621–630

Abstract: ... the JNK/c-Jun/Slug pathway, and with the form of its enzymatic activity. Clinical samples confirmed ... that B4GALNT1 expression was upregulated in LUAD, and B4GALNT1 was correlated with c-Jun/Slug expression ... suggest that B4GALNT1 promotes progression and metastasis of LUAD through activating JNK/c-Jun/Slug ...

Abstract	Lung adenocarcinoma (LUAD) is one of the most common types of cancer and has a low survival rate. β-1,4-N-Acetyl galactosaminyltransferase 1 (B4GALNT1), which is involved in the synthesis of complex gangliosides, is highly expressed in the progression of various cancers. This study aimed to elucidate the biological functions of B4GALNT1 in LUAD progression and metastasis. We observed that B4GALNT1 overexpression showed enhanced cell migration and invasion in vitro, and promoted tumor metastasis, with reduced survival in mice. Mechanistically, B4GALNT1 regulated metastatic potential of LUAD through activating the JNK/c-Jun/Slug pathway, and with the form of its enzymatic activity. Clinical samples confirmed that B4GALNT1 expression was upregulated in LUAD, and B4GALNT1 was correlated with c-Jun/Slug expression, lymph node involvement, advanced clinical stage, and reduced overall survival. Collectively, our results suggest that B4GALNT1 promotes progression and metastasis of LUAD through activating JNK/c-Jun/Slug signaling, and with the form of its enzymatic activity.
MeSH term(s)	Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/pathology ; Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation/genetics ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Heterografts ; Humans ; JNK Mitogen-Activated Protein Kinases/genetics ; MAP Kinase Kinase 4/genetics ; Male ; Mice ; N-Acetylgalactosaminyltransferases/genetics ; Neoplasm Metastasis ; Signal Transduction ; Snail Family Transcription Factors/genetics
Chemical Substances	SNAI1 protein, human ; Snail Family Transcription Factors ; N-Acetylgalactosaminyltransferases (EC 2.4.1.-) ; B4galnt1 protein, human (EC 2.4.1.165) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2020-12-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgaa141
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