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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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Zs.A 2142: Show issues

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Article: Down-regulation of Jun induces senescence through destabilizing chromatin in osteoarthritis chondrocytes.

Xie, Ting / Ren, Xunshan / Zhuang, Huangming / Jiang, Fuze / Zhang, Yuelong / Zhou, Panghu

American journal of translational research

2023 Volume 15, Issue 7, Page(s) 4873–4886

Abstract: ... Using cytoHubba in Cytoscape, we identified Jun as the hub-ASDEG for OA chondrocytes. We confirmed ... the downregulation of Jun in OA rats and senescent chondrocytes by immunohistochemistry and quantitative ... were observed in chondrocytes treated with siRNA against Jun. Mechanistically, we observed micronuclei ...

Abstract	Objective: Osteoarthritis (OA) is the most common degenerative joint disease leading to disability worldwide. Cellular senescence is considered to be a fundamental pathogenic mechanism in the development of OA and has attracted increasing attention. However, regulatory mechanisms underlying chondrocyte senescence in OA remain unclear. Methods: Bioinformatic methods were used to screen key genes. Immunohistochemistry and the quantitative reverse transcription polymerase chain reaction were used to evaluate gene expression. RNA intervention experiments were performed to explore the functions of key genes. Results: We used 494 aging-associated genes provided by the Aging Atlas to identify the co-expression modules associated with age and OA. Thirty age-associated differentially expressed genes (ASDEGs) were identified. Using cytoHubba in Cytoscape, we identified Jun as the hub-ASDEG for OA chondrocytes. We confirmed the downregulation of Jun in OA rats and senescent chondrocytes by immunohistochemistry and quantitative reverse transcription polymerase chain reaction, respectively. Inhibition of proliferation and accelerated senescence were observed in chondrocytes treated with siRNA against Jun. Mechanistically, we observed micronuclei formation and reduced expression of H3K9me3 and heterochromatin protein 1gamma in siRNA-Jun-treated chondrocytes, indicating that destabilization of chromatin occurred during this treatment. Conclusion: Jun plays a crucial role in OA development and causes senescence by destabilizing chromatin in chondrocytes. These findings provide new insights into OA progression and suggest promising therapeutic targets.
Language	English
Publishing date	2023-07-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2471058-1
ISSN	1943-8141
ISSN	1943-8141
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Article ; Online: Jun/Fos promotes migration and invasion of hepatocellular carcinoma cells by enhancing BORIS promoter activity.

Xian, Longjun / Xiong, Yimei / Qin, Lu / Wei, Ling / Zhou, Siqi / Wang, Qinda / Fu, Qiang / Chen, Mingmei / Qin, Yang

The international journal of biochemistry & cell biology

2024 Volume 169, Page(s) 106540

Abstract: ... engages in interactions with the Hippo pathway. Thus, we attempt to prove whether Jun and Fos, a major ... revealed the existence of binding sites for Jun and Fos within the BORIS promoter. Through a series ... of overexpression and knockdown experiments, we corroborated that Jun and Fos have the capacity to augment BORIS ...

Abstract	The Brother of the Regulator of Imprinted Sites (BORIS), as a specific indicator of hepatocellular carcinoma, exhibits a significant increase in expression. However, its upstream regulatory network remains enigmatic. Previous research has indicated a strong correlation between the Hippo pathway and the progression of hepatocellular carcinoma. It is well established that the Activator Protein-1 (AP-1) frequently engages in interactions with the Hippo pathway. Thus, we attempt to prove whether Jun and Fos, a major member of the AP-1 family, are involved in the regulation of BORIS expression. Bioinformatics analysis revealed the existence of binding sites for Jun and Fos within the BORIS promoter. Through a series of overexpression and knockdown experiments, we corroborated that Jun and Fos have the capacity to augment BORIS expression, thereby fostering the migration and invasion of hepatocellular carcinoma cells. Moreover, Methylation-Specific PCR and Bisulfite Sequencing PCR assays revealed that Jun and Fos do not have a significant impact on the demethylation of the BORIS promoter. However, luciferase reporter and chromatin immunoprecipitation experiments substantiated that Jun and Fos could directly bind to the BORIS promoter, thereby enhancing its transcription. In conclusion, these results suggest that Jun and Fos can promote the development of hepatocellular carcinoma by directly regulating the expression of BORIS. These findings may provide experimental evidence positioning BORIS as a novel target for the clinical intervention of hepatocellular carcinoma.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Transcription Factor AP-1/genetics ; Transcription Factor AP-1/metabolism ; Liver Neoplasms/pathology ; Cell Line ; Promoter Regions, Genetic/genetics
Chemical Substances	Transcription Factor AP-1
Language	English
Publishing date	2024-01-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2024.106540
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Zs.A 431: Show issues

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Article ; Online: S100P facilitates LUAD progression via PKA/c-Jun-mediated tumor-associated macrophage recruitment and polarization.

Gao, Lu / Bai, Ying / Zhou, Jiawei / Liang, Chao / Dong, Yunjia / Han, Tao / Liu, Yafeng / Guo, Jianqiang / Wu, Jing / Hu, Dong

Cellular signalling

2024 , Page(s) 111179

Abstract: ... of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment ... and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes ... that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting ...

Abstract	S100P, a member of the S100 calcium-binding protein family, is closely associated with abnormal proliferation, invasion, and metastasis of various cancers. However, its role in the lung adenocarcinoma (LUAD) tumor microenvironment (TME) remains unclear. In this study, we observed specific expression of S100P on tumor cells in LUAD patients through tissue immunofluorescence analysis. Furthermore, this expression was strongly correlated with the recruitment and polarization of tumor-associated macrophages (TAMs). Bioinformatics analysis revealed that high S100P expression is associated with poorer overall survival in LUAD patients. Subsequently, a subcutaneous mouse model demonstrated that S100P promotes recruitment and polarization of TAMs towards the M2 type. Finally, in vitro studies on LUAD cells revealed that S100P enhances the secretion of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes the ability of TAMs to infiltrate and polarize towards the M2 phenotype. In conclusion, our study demonstrates that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting in the production of various cytokines. Considering these findings, S100P holds promise as an important diagnostic marker and potential therapeutic target for LUAD.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2024.111179
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Zs.A 2579: Show issues

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Article ; Online: Correction: Ubiquitous mitochondrial creatine kinase promotes the progression of gastric cancer through a JNK-MAPK/JUN/HK2 axis regulated glycolysis.

Mi, Yushuai / Li, Quanhui / Liu, Bingtian / Wang, Dehai / Liu, Ziping / Wang, Tianshi / Wang, Yuan / Zang, Yifeng / Zhou, Yan / Wen, Yugang / Ding, Yinlu

Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association

2024 Volume 27, Issue 3, Page(s) 646–648

Language	English
Publishing date	2024-03-22
Publishing country	Japan
Document type	Published Erratum
ZDB-ID	1463526-4
ISSN	1436-3305 ; 1436-3291
ISSN (online)	1436-3305
ISSN	1436-3291
DOI	10.1007/s10120-024-01490-w
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Zs.A 5290: Show issues

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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: NNMT contributes to high metastasis of triple negative breast cancer by enhancing PP2A/MEK/ERK/c-Jun/ABCA1 pathway mediated membrane fluidity.

Wang, Yanzhong / Zhou, Xi / Lei, Yinjiao / Chu, Yadong / Yu, Xingtong / Tong, Qingchao / Zhu, Tao / Yu, Haitao / Fang, Sining / Li, Guoli / Wang, Linbo / Wang, Gavin Y / Xie, Xinyou / Zhang, Jun

Cancer letters

2022 Volume 547, Page(s) 215884

Abstract: ... levels in the cytoplasm and cell membrane. Mechanistically, NNMT activated MEK/ERK/c-Jun/ABCA1 pathway ...

Abstract	Elucidating the mechanism for high metastasis capacity of triple negative breast cancers (TNBC) is crucial to improve treatment outcomes of TNBC. We have recently reported that nicotinamide N-methyltransferase (NNMT) is overexpressed in breast cancer, especially in TNBC, and predicts poor survival of patients undergoing chemotherapy. Here, we aimed to determine the function and mechanism of NNMT on metastasis of TNBC. Additionally, analysis of public datasets indicated that NNMT is involved in cholesterol metabolism. In vitro, NNMT overexpression promoted migration and invasion of TNBCs by reducing cholesterol levels in the cytoplasm and cell membrane. Mechanistically, NNMT activated MEK/ERK/c-Jun/ABCA1 pathway by repressing protein phosphatase 2A (PP2A) activity leading to cholesterol efflux and membrane fluidity enhancement, thereby promoting the epithelial-mesenchymal transition (EMT) of TNBCs. In vivo, the metastasis capacity of TNBCs was weakened by targeting NNMT. Collectively, our findings suggest a new molecular mechanism involving NNMT in metastasis and poor survival of TNBC mediated by PP2A and affecting cholesterol metabolism.
MeSH term(s)	Humans ; ATP Binding Cassette Transporter 1/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cholesterol ; Epithelial-Mesenchymal Transition ; Membrane Fluidity ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Neoplasm Metastasis ; Nicotinamide N-Methyltransferase/metabolism ; Protein C/metabolism ; Protein C/therapeutic use ; Triple Negative Breast Neoplasms/metabolism
Chemical Substances	ABCA1 protein, human ; ATP Binding Cassette Transporter 1 ; Cholesterol (97C5T2UQ7J) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Nicotinamide N-Methyltransferase (EC 2.1.1.1) ; NNMT protein, human (EC 2.1.1.1) ; Protein C
Language	English
Publishing date	2022-08-19
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.215884
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Zs.A 1177: Show issues

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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: JUN mediates glucocorticoid resistance by stabilizing HIF1a in T cell acute lymphoblastic leukemia.

Zhang, Zhijie / Shi, Jiangzhou / Wu, Qifang / Zhang, Zijian / Liu, Xiaoyan / Ren, Anqi / Zhao, Guanlin / Dong, Ge / Wu, Han / Zhao, Jiaxuan / Zhao, Yuan / Hu, Jia / Li, Hui / Zhang, Tongcun / Zhou, Fuling / Zhu, Haichuan

iScience

2023 Volume 26, Issue 11, Page(s) 108242

Abstract: ... are poorly understood. Here, we demonstrated that the expression of JUN was regulated in Dex-resistant ... T-ALL cell lines and patient samples. JUN knockdown increased the sensitivity to Dex. Moreover ... the survival data showed that high expression of JUN related to poor prognosis of T-ALL patients ...

Abstract	Dexamethasone (Dex) plays a critical role in T-ALL treatment, but the mechanisms of Dex resistance are poorly understood. Here, we demonstrated that the expression of JUN was regulated in Dex-resistant T-ALL cell lines and patient samples. JUN knockdown increased the sensitivity to Dex. Moreover, the survival data showed that high expression of JUN related to poor prognosis of T-ALL patients. Then, we generated dexamethasone-resistant clones and conducted RNA-seq and ATAC-seq. We demonstrated that the upregulation of JUN was most significant and regulated by JNK pathway in Dex-resistant cells. High-throughput screening showed that HIF1α inhibitors synergized with Dex could enhance Dex resistance cells death
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108242
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Article: Liquiritin exhibits anti-acute lung injury activities through suppressing the JNK/Nur77/c-Jun pathway.

Zhou, Hongling / Yang, Tangjia / Lu, Zibin / He, Xuemei / Quan, Jingyu / Liu, Shanhong / Chen, Yuyao / Wu, Kangtai / Cao, Huihui / Liu, Junshan / Yu, Linzhong

Chinese medicine

2023 Volume 18, Issue 1, Page(s) 35

Abstract: ... the enzyme linked immunosorbent assay. Western blot analysis was used to detect the expression of JNK/Nur77/c-Jun related proteins ... while electrophoretic mobility shift assay was used to examine the c-Jun DNA binding activity.: Results: LQ has significant ... Tyr185), p-Nur77 (Ser351) and p-c-Jun (Ser63), while elevated the Nur77 expression level. Inhibition ...

Abstract	Background: Licorice (Glycyrrhiza uralensis Fisch.), a well-known traditional medicine, is traditionally used for the treatment of respiratory disorders, such as cough, sore throat, asthma and bronchitis. We aim to investigate the effects of liquiritin (LQ), the main bioactive compound in licorice against acute lung injury (ALI) and explore the potential mechanism. Methods: Lipopolysaccharide (LPS) was used to induce inflammation in RAW264.7 cells and zebrafish. Intratracheal instillation of 3 mg/kg of LPS was used for induction an ALI mice model. The concentrations of IL-6 and TNF-α were tested using the enzyme linked immunosorbent assay. Western blot analysis was used to detect the expression of JNK/Nur77/c-Jun related proteins. Protein levels in bronchoalveolar lavage fluid (BALF) was measured by BCA protein assay. The effect of JNK on Nur77 transcriptional activity was determined by luciferase reporter assay, while electrophoretic mobility shift assay was used to examine the c-Jun DNA binding activity. Results: LQ has significant anti-inflammatory effects in zebrafish and RAW264.7 cells. LQ inhibited the expression levels of p-JNK (Thr183/Tyr185), p-Nur77 (Ser351) and p-c-Jun (Ser63), while elevated the Nur77 expression level. Inhibition of JNK by a specific inhibitor or small interfering RNA enhanced the regulatory effect of LQ on Nur77/c-Jun, while JNK agonist abrogated LQ-mediated effects. Moreover, Nur77-luciferase reporter activity was suppressed after JNK overexpression. The effects of LQ on the expression level of c-Jun and the binding activity of c-Jun with DNA were attenuated after Nur77 siRNA treatment. LQ significantly ameliorated LPS-induced ALI with the reduction of lung water content and BALF protein content, the downregulation of TNF-α and IL-6 levels in lung BALF and the suppression of JNK/Nur77/c-Jun signaling, which can be reversed by a specific JNK agonist. Conclusion: Our results indicated that LQ exerts significant protective effects against LPS-induced inflammation both in vivo and in vitro via suppressing the activation of JNK, and consequently inhibiting the Nur77/c-Jun signaling pathway. Our study suggests that LQ may be a potential therapeutic candidate for ALI and inflammatory disorders.
Language	English
Publishing date	2023-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2260322-0
ISSN	1749-8546
ISSN	1749-8546
DOI	10.1186/s13020-023-00739-3
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