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Article: JUN

Zhang, Ming / Xu, Pei / Sun, Xiaolin / Zhang, Chen / Shi, Xiang / Li, Jancheng / Jiang, Jingyi / Chen, Chen / Zhang, Yani / Chen, Guohong / Li, Bichun / Zuo, Qisheng

Cytotechnology

2021 Volume 73, Issue 1, Page(s) 101–113

Abstract: The sex determination and control of poultry is a key problem in production and scientific research despite few studies on regulatory factors, especially transcription factors in sex determination. In the early stage of this study, high-throughput ... ...

Abstract	The sex determination and control of poultry is a key problem in production and scientific research despite few studies on regulatory factors, especially transcription factors in sex determination. In the early stage of this study, high-throughput sequencing was used to screen the differentially expressed gene
Language	English
Publishing date	2021-01-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1035772-5
ISSN	0920-9069
ISSN	0920-9069
DOI	10.1007/s10616-020-00447-y
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Zs.A 2604: Show issues

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Article ; Online: The chromatin remodeling factor Arid1a cooperates with Jun/Fos to promote osteoclastogenesis by epigenetically upregulating Siglec15 expression.

Zhang, Yongxing / Sun, Hangxiang / Huang, Fei / Chen, Yang / Ding, Xiying / Zhou, Chenhe / Wu, Yan / Zhang, Qing / Ma, Xiao / Wang, Jun / Yue, Rui / Shen, Li / Sun, Xuxu / Ye, Zhaoming

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2024

Abstract: ... Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion ...

Abstract	Osteoporosis is characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-related bone formation, particularly increased osteoclastogenesis. However, the mechanisms by which epigenetic factors regulate osteoclast precursor differentiation during osteoclastogenesis remain poorly understood. Here, we show that the specific knockout of the chromatin remodeling factor Arid1a in bone marrow-derived macrophages (BMDMs) results in increased bone mass. The loss of Arid1a in BMDM inhibits cell-cell fusion and maturation of osteoclast precursors, thereby suppressing osteoclast differentiation. Mechanistically, Arid1a increases the chromatin access in the gene promoter region of sialic acid-binding Ig-like lectin 15 (Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion of osteoclast differentiation. However, the loss of Arid1a reprograms the chromatin structure to restrict Siglec15 expression in osteoclast precursors, thereby inhibiting BMDM differentiation into mature osteoclasts. Deleting Arid1a after ovariectomy (a model for postmenopausal bone loss) alleviated bone loss and maintained bone mass. In summary, epigenetic reprogramming mediated by Arid1a loss suppresses osteoclast differentiation and may serve as a promising therapeutic strategy for treating bone loss diseases.
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Journal Article
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1093/jbmr/zjae042
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Article ; Online: Overexpression of c-Jun inhibits erastin-induced ferroptosis in Schwann cells and promotes repair of facial nerve function.

Gao, Dekun / Huang, Yuyu / Sun, Xiayu / Yang, Jun / Chen, Jianyong / He, Jingchun

Journal of cellular and molecular medicine

2022 Volume 26, Issue 8, Page(s) 2191–2204

Abstract: Myelin undergoes various changes after nerve injury, and c-Jun has a close relationship ... with Schwann cells (SCs). However, it remains unclear whether c-Jun can be involved in nerve repair by regulating ... of ferroptosis-related proteins and c-Jun by immunofluorescence and Western blot. Then, we cultured RSC 96 and ...

Abstract	Myelin undergoes various changes after nerve injury, and c-Jun has a close relationship with Schwann cells (SCs). However, it remains unclear whether c-Jun can be involved in nerve repair by regulating ferroptosis. To explore this, we first set up a facial nerve injury model and detected the changes of ferroptosis-related proteins and c-Jun by immunofluorescence and Western blot. Then, we cultured RSC 96 and pSCs, and studied the potential regulatory relationships by a combination of experimental methods such as CCK-8, ELISA, immunofluorescence, qRT-PCR, Western blot and viral transfection. Finally, we corroborated the role of c-Jun through animal experiments. Our experiments revealed that ferroptosis occurs after facial nerve injury. Erastin decreased GPX4, c-Jun proteins and GSH content, while PTGS2, NRF2, HO-1 proteins, MDA, Fe
MeSH term(s)	Animals ; Facial Nerve/metabolism ; Facial Nerve Injuries ; Ferroptosis ; NF-E2-Related Factor 2/metabolism ; Peripheral Nerve Injuries ; Piperazines ; Schwann Cells/metabolism ; Signal Transduction
Chemical Substances	NF-E2-Related Factor 2 ; Piperazines ; erastin
Language	English
Publishing date	2022-02-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.17241
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Zs.A 5752: Show issues

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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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Zs.A 1494: Show issues

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Article ; Online: Inhibition of ATM promotes PD-L1 expression by activating JNK/c-Jun/TNF-α signaling axis in triple-negative breast cancer.

Liu, Chenying / Qian, Xiaolong / Yu, Chunyan / Xia, Xiaoqing / Li, Jiazhen / Li, Yaqing / Xie, Yongjie / Gao, Guangshen / Song, Yuanming / Zhang, Meiyan / Xue, Huiqin / Wang, Xiaozi / Sun, Hui / Liu, Jing / Deng, Weimin / Guo, Xiaojing

Cancer letters

2024 Volume 586, Page(s) 216642

Abstract: ... inhibits TNF-α via inactivating JNK/c-Jun by scRNA-seq, Western blot and luciferase reporter assays ...

Abstract	Triple-negative breast cancer (TNBC) is a heterogeneous subtype of breast cancer. Anti-PD-1/PD-L1 treatment for advanced TNBC is still limited to PD-L1-positive patients. Ataxia telangiectasia mutated (ATM) is a switch molecule for homologous recombination and repair. In this study, we found a significant negative correlation between ATM and PD-L1 in 4 TNBC clinical specimens by single-cell RNA sequencing (scRNA-seq), which was confirmed by immunochemical staining in 86 TNBC specimens. We then established ATM knockdown TNBC stable cell lines to perform in vitro studies and animal experiments, proving the negative regulation of PD-L1 by ATM via suppression of tumor necrosis factor-alpha (TNF-α), which was confirmed by cytokine array analysis of TNBC cell line and analysis of clinical specimens. We further found that ATM inhibits TNF-α via inactivating JNK/c-Jun by scRNA-seq, Western blot and luciferase reporter assays. Finally, we identified a negative correlation between changes in phospho-ATM
MeSH term(s)	Animals ; Humans ; Ataxia Telangiectasia ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; B7-H1 Antigen/metabolism ; Cytokines/metabolism ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; ATM protein, human (EC 2.7.11.1) ; B7-H1 Antigen ; CD274 protein, human ; Cytokines ; Tumor Necrosis Factor-alpha ; JUN protein, human
Language	English
Publishing date	2024-01-24
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2024.216642
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Zs.A 1177: Show issues

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Article: Reply to Comment on "Jun, S.Y.; et al. Tumor Budding and Poorly Differentiated Clusters in Small Intestinal Adenocarcinoma"

Jun, Sun-Young / Hong, Seung-Mo

Cancers

2020 Volume 12, Issue 10

Abstract: We thank Giuffrida et al [ ... ]. ...

Abstract	We thank Giuffrida et al [...].
Language	English
Publishing date	2020-10-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12102987
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Article ; Online: c-Jun-mediated JMJD6 restoration enhances resistance of liver cancer to radiotherapy through the IL-4-activated ERK pathway.

Liu, Yong / Sui, Aixia / Sun, Jirui / Wu, Yifan / Liu, Fuquan / Yang, Yang

Cell biology international

2023 Volume 47, Issue 8, Page(s) 1392–1405

Abstract: ... by radioresistance. In this study, we attempt to delineate the possible molecular mechanism of c-Jun-regulated ... axis in radioresistance of liver cancer. The expression of c-Jun was quantified in liver cancer tissues ... and cell lines, and the results indicated that c-Jun was upregulated in liver cancer tissues and cells ...

Abstract	Radiotherapy is widely used in the treatment of liver cancer, but the efficacy can be limited by radioresistance. In this study, we attempt to delineate the possible molecular mechanism of c-Jun-regulated Jumonji domain-containing protein 6/interleukin 4/extracellular signal-regulated kinase (JMJD6/IL-4/ERK) axis in radioresistance of liver cancer. The expression of c-Jun was quantified in liver cancer tissues and cell lines, and the results indicated that c-Jun was upregulated in liver cancer tissues and cells. We further illustrated the role of c-Jun following gain- and loss-of-function strategies in malignant phenotypes of liver cancer cells. It was established that c-Jun elevated JMJD6 expression and augmented the malignancy and aggressiveness of liver cancer cells. The in vivo effects of c-Jun on radioresistance in liver cancer were validated in nude mice, in response to IL-4 knockdown or the ERK pathway inhibitor, PD98059. In the presence of JMJD6 upregulation, the expression of IL-4 was elevated in mice with liver cancer, which enhanced the radiation resistance. Moreover, knockdown of IL-4 inactivated the ERK pathway, thereby reversing the radiation resistance caused by overexpressed JMJD6 in tumor-bearing mice. Taken together, c-Jun augments the radiation resistance in liver cancer by activating the ERK pathway through JMJD6-upregulated IL-4 transcription.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Interleukin-4/pharmacology ; Liver Neoplasms/radiotherapy ; MAP Kinase Signaling System ; Mice, Nude ; Radiation Tolerance
Chemical Substances	Interleukin-4 (207137-56-2)
Language	English
Publishing date	2023-04-18
Publishing country	England
Document type	Journal Article
ZDB-ID	1143453-3
ISSN	1095-8355 ; 1065-6995
ISSN (online)	1095-8355
ISSN	1065-6995
DOI	10.1002/cbin.12026
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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: JNK-JUN-NCOA4 axis contributes to chondrocyte ferroptosis and aggravates osteoarthritis via ferritinophagy.

Sun, Kai / Hou, Liangcai / Guo, Zhou / Wang, Genchun / Guo, Jiachao / Xu, Jingting / Zhang, Xiong / Guo, Fengjing

Free radical biology & medicine

2023 Volume 200, Page(s) 87–101

Abstract: ... in a JNK-JUN signaling-dependent manner in which JUN could directly bind to the promoter of Ncoa4 and ... In addition, inhibition of JNK-JUN-NCOA4 axis by SP600125, a specific inhibitor of JNK, attenuated development ... of post-traumatic OA. This work highlights the role of JNK-JUN-NCOA4 axis and ferritinophagy ...

Abstract	Interruption of iron homeostasis is correlated with cell ferroptosis and degenerative diseases. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy has been reported as a vital mechanism to control cellular iron levels, but its impact on osteoarthritis (OA) pathology and the underline mechanism are unknown. Herein we aimed to investigate the role and regulatory mechanism of NCOA4 in chondrocyte ferroptosis and OA pathogenesis. We demonstrated that NCOA4 was highly expressed in cartilage of patients with OA, aged mice, post-traumatic OA mice, and inflammatory chondrocytes. Importantly, Ncoa4 knockdown inhibited IL-1β-induced chondrocyte ferroptosis and extracellular matrix degradation. Contrarily, overexpression of NCOA4 promoted chondrocyte ferroptosis and the delivery of Ncoa4 adeno-associated virus 9 into knee joint of mice aggravated post-traumatic OA. Mechanistic study revealed that NCOA4 was upregulated in a JNK-JUN signaling-dependent manner in which JUN could directly bind to the promoter of Ncoa4 and initial the transcription of Ncoa4. NCOA4 could interact with ferritin and increase autophagic degradation of ferritin and iron levels, which caused chondrocyte ferroptosis and extracellular matrix degradation. In addition, inhibition of JNK-JUN-NCOA4 axis by SP600125, a specific inhibitor of JNK, attenuated development of post-traumatic OA. This work highlights the role of JNK-JUN-NCOA4 axis and ferritinophagy in chondrocyte ferroptosis and OA pathogenesis, suggesting this axis as a potential target for OA treatment.
MeSH term(s)	Animals ; Mice ; Chondrocytes/metabolism ; Ferroptosis/genetics ; Osteoarthritis/metabolism ; Ferritins/genetics ; Ferritins/metabolism ; Transcription Factors/metabolism ; Iron/metabolism ; Nuclear Receptor Coactivators/genetics ; Nuclear Receptor Coactivators/metabolism
Chemical Substances	Ferritins (9007-73-2) ; Transcription Factors ; Iron (E1UOL152H7) ; NcoA4 protein, mouse ; Nuclear Receptor Coactivators
Language	English
Publishing date	2023-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2023.03.008
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