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Article ; Online: Reprogramming Stars #7: Dynamic Pluripotent Stem Cell States and Their Applications-An Interview with Dr. Jun Wu.

Wu, Jun / Pereira, Carlos-Filipe / Lu, Yuancheng Ryan

2022 Volume 24, Issue 3, Page(s) 105–110

MeSH term(s)	Cell Differentiation ; Cellular Reprogramming ; Induced Pluripotent Stem Cells ; Pluripotent Stem Cells
Language	English
Publishing date	2022-05-14
Publishing country	United States
Document type	Interview
ZDB-ID	2542436-1
ISSN	2152-4998 ; 1557-7457 ; 2152-4971
ISSN (online)	2152-4998 ; 1557-7457
ISSN	2152-4971
DOI	10.1089/cell.2022.29064.jc
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Zs.A 5452: Show issues

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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: 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: 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: 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: Retraction notice to " Ophiopogonin B induces the autophagy and apoptosis of colon cancer cells by activating JNK/c-Jun signaling pathway" [Biomed. Pharmacother. Volume 108, December 2018, Pages 1208-1215].

Gao, Guang-Yi / Ma, Jun / Lu, Peng / Jiang, Xuan / Chang, Cheng

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 163, Page(s) 114768

Language	English
Publishing date	2023-05-09
Publishing country	France
Document type	Journal Article ; Retraction of Publication
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.114768
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Ud II Zs.198: Show issues

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Article ; Online: Retraction Note: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer.

Lin, Zhuo-Yuan / Chen, Guo / Zhang, Yan-Qiong / He, Hui-Chan / Liang, Yu-Xiang / Ye, Jian-Heng / Liang, Ying-Ke / Mo, Ru-Jun / Lu, Jian-Ming / Zhuo, Yang-Jia / Zheng, Yu / Jiang, Fu-Neng / Han, Zhao-Dong / Wu, Shu-Lin / Zhong, Wei-de / Wu, Chin-Lee

Molecular cancer

2023 Volume 22, Issue 1, Page(s) 56

Language	English
Publishing date	2023-03-20
Publishing country	England
Document type	Retraction of Publication
ZDB-ID	2091373-4
ISSN	1476-4598 ; 1476-4598
ISSN (online)	1476-4598
ISSN	1476-4598
DOI	10.1186/s12943-023-01763-5
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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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Article ; Online: Dach1 deficiency drives alveolar epithelium apoptosis in pulmonary fibrosis via modulating C-Jun/Bim activity.

Lu, Yanjiao / Tang, Kum / Wang, Shanshan / Tian, Zhen / Fan, Yan / Li, Boyu / Wang, Meijia / Zhao, Jianping / Xie, Jungang

Translational research : the journal of laboratory and clinical medicine

2023 Volume 257, Page(s) 54–65

Abstract: ... combined with C-Jun protooncogene selectively bound to the promoter of B-cell lymphoma 2 interacting ...

Abstract	Dysregulation of type II alveolar epithelial cells (AECII) plays a vital role in the initiation and development of pulmonary fibrosis (PF). Dachshund homolog 1 (Dach1), frequently expressed in epithelial cells with stem cell potential, controls cell proliferation, apoptosis, and cell cycle in tissue development and disease process. In this study, we demonstrated that the lungs collected from PF patients and mice of Bleomycin (BLM)-treated were characterized by low expression of Dachshund homolog 1 (Dach1), especially in AECII. Dach1 deficiency in the alveolar epithelium exacerbated PF in BLM-treated mice, as evidenced by reduced pulmonary function and increased expression of fibrosis markers. Rather, treatment with lung-specific overexpression of Dach1 alleviated histopathological damage, lung compliance, and fibrosis in BLM-treated mice. Moreover, overexpression of Dach1 could inhibit epithelial apoptosis in vitro. Conversely, primary AECII with Dach1 depletion were more susceptible to apoptosis in vivo. Mechanically, Dach1 combined with C-Jun protooncogene selectively bound to the promoter of B-cell lymphoma 2 interacting mediators of cell death (Bim), by which it repressed Bim expression and alleviated epithelial apoptosis. Taken together, our data support that Dach1 in AECII contributes to the progression of PF and may be a viable target for the prevention and treatment of PF.
MeSH term(s)	Animals ; Mice ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/pathology ; Apoptosis ; Bleomycin/toxicity ; Bleomycin/metabolism ; Epithelium/pathology ; Eye Proteins/genetics ; Lung/pathology ; Pulmonary Fibrosis/metabolism
Chemical Substances	Bleomycin (11056-06-7) ; Dach1 protein, mouse ; Eye Proteins
Language	English
Publishing date	2023-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2023.01.006
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Article ; Online: Oleanolic acid attenuates hydrogen peroxide-induced apoptosis of IPEC-J2 cells through suppressing c-Jun and MAPK pathway.

Hu, Mingyang / Zhang, Lei / Jia, Hongpeng / Xue, Chenyu / Zhao, Lu / Dong, Na / Shan, Anshan

Journal of biochemical and molecular toxicology

2023 Volume 38, Issue 1, Page(s) e23538

Abstract: Oleanolic acid (OA) is a natural triterpenoid with therapeutic potential for a multitude of diseases. However, the precise mechanism by which OA influences stress-induced apoptosis of intestinal epithelial cells remains elusive. Therefore, the effect of ... ...

Abstract	Oleanolic acid (OA) is a natural triterpenoid with therapeutic potential for a multitude of diseases. However, the precise mechanism by which OA influences stress-induced apoptosis of intestinal epithelial cells remains elusive. Therefore, the effect of OA on intestinal diseases under stressful conditions and its possible mechanisms have been investigated. In a hydrogen peroxide (H
MeSH term(s)	Hydrogen Peroxide/pharmacology ; Hydrogen Peroxide/metabolism ; Oleanolic Acid/pharmacology ; Cell Line ; Apoptosis ; Oxidative Stress ; Epithelial Cells/metabolism
Chemical Substances	Hydrogen Peroxide (BBX060AN9V) ; Oleanolic Acid (6SMK8R7TGJ)
Language	English
Publishing date	2023-09-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	1410020-4
ISSN	1099-0461 ; 1095-6670
ISSN (online)	1099-0461
ISSN	1095-6670
DOI	10.1002/jbt.23538
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