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Article: c-Jun as a one-way valve at the naive to primed interface.

Li, Dongwei / Luo, Ling / Guo, Lin / Wu, Chuman / Zhang, Ran / Peng, Yuling / Wu, Menghua / Kuang, Junqi / Li, Yan / Zhang, Yudan / Xie, Jun / Xie, Wenxiu / Mao, Rui / Ma, Gang / Fu, Xiuling / Chen, Jiekai / Hutchins, Andrew P / Pei, Duanqing

Cell & bioscience

2023 Volume 13, Issue 1, Page(s) 191

Abstract: Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene ... However, its role in early embryonic development remains unknown.: Results: Here, we show that c-Jun acts ... as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced ...

Abstract	Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown. Results: Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient. Conclusions: The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
Language	English
Publishing date	2023-10-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2593367-X
ISSN	2045-3701
ISSN	2045-3701
DOI	10.1186/s13578-023-01141-0
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Article ; Online: c-Jun as a one-way valve at the naive to primed interface

Dongwei Li / Ling Luo / Lin Guo / Chuman Wu / Ran Zhang / Yuling Peng / Menghua Wu / Junqi Kuang / Yan Li / Yudan Zhang / Jun Xie / Wenxiu Xie / Rui Mao / Gang Ma / Xiuling Fu / Jiekai Chen / Andrew P. Hutchins / Duanqing Pei

Cell & Bioscience, Vol 13, Iss 1, Pp 1-

2023 Volume 16

Abstract: Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor ... However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way ... valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during ...

Abstract	Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient. Conclusions The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
Keywords	EpiSCs ; c-Jun ; Naïve to primed transition ; Primed to naïve transition ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: JunB: a paradigm for Jun family in immune response and cancer.

Ren, Fu-Jia / Cai, Xiao-Yu / Yao, Yao / Fang, Guo-Ying

Frontiers in cellular and infection microbiology

2023 Volume 13, Page(s) 1222265

Abstract: Jun B proto-oncogene (JunB) is a crucial member of dimeric activator protein-1 (AP-1) complex ...

Abstract	Jun B proto-oncogene (JunB) is a crucial member of dimeric activator protein-1 (AP-1) complex, which plays a significant role in various physiological processes, such as placental formation, cardiovascular development, myelopoiesis, angiogenesis, endochondral ossification and epidermis tissue homeostasis. Additionally, it has been reported that JunB has great regulatory functions in innate and adaptive immune responses by regulating the differentiation and cytokine secretion of immune cells including T cells, dendritic cells and macrophages, while also facilitating the effector of neutrophils and natural killer cells. Furthermore, a growing body of studies have shown that JunB is involved in tumorigenesis through regulating cell proliferation, differentiation, senescence and metastasis, particularly affecting the tumor microenvironment through transcriptional promotion or suppression of oncogenes in tumor cells or immune cells. This review summarizes the physiological function of JunB, its immune regulatory function, and its contribution to tumorigenesis, especially focusing on its regulatory mechanisms within tumor-associated immune processes.
MeSH term(s)	Female ; Pregnancy ; Humans ; Placenta ; Neoplasms ; Carcinogenesis ; Cell Transformation, Neoplastic ; Immunity ; Tumor Microenvironment ; Transcription Factors
Chemical Substances	JunB protein, human ; Transcription Factors
Language	English
Publishing date	2023-09-04
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2023.1222265
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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: NAP1L1 promotes tumor proliferation through HDGF/C-JUN signaling in ovarian cancer.

Xiaohua Zhu / Xie, YingYing / Huang, Wenyan / Chen, Zigui / Guo, SuiQun

BMC cancer

2022 Volume 22, Issue 1, Page(s) 339

Abstract: ... with jun proto-oncogene (C-JUN), an oncogenic transformation factor that induces the expression of cyclin D1 (CCND1 ... Overexpressed HDGF in NAP1L1 knockdown OC cells not only increased the expression of C-JUN and CCND1 ... the proliferation of OC, and this process of triggered proliferation may contribute to the activation of HDGF/C-JUN ...

Abstract	Background: Nucleosome assembly protein 1-like 1 (NAP1L1) is highly expressed in various types of cancer and plays an important role in carcinogenesis, but its specific role in tumor development and progression remains largely unknown. In this study, we suggest the potential of NAP1L1 as a prognostic biomarker and therapeutic target for the treatment of ovarian cancer (OC). Methods: In our study, a tissue microarray (TMA) slide containing specimens from 149 patients with OC and 11 normal ovarian tissues underwent immunohistochemistry (IHC) to analyze the correlation between NAP1L1 expression and clinicopathological features. Loss-of- function experiments were performed by transfecting siRNA and following lentiviral gene transduction into SKOV3 and OVCAR3 cells. Cell proliferation and the cell cycle were assessed by the Cell Counting Kit-8, EDU assay, flow cytometry, colony formation assay, and Western blot analysis. In addition, co-immunoprecipitation (Co-IP) and immunofluorescence assays were performed to confirm the relationship between NAP1L1 and its potential targets in SKOV3/OVCAR3 cells. Results: High expression of NAP1L1 was closely related to poor clinical outcomes in OC patients. After knocking down NAP1L1 by siRNA or shRNA, both SKOV3 and OVCAR3 cells showed inhibition of cell proliferation, blocking of the G1/S phase, and increased apoptosis in vitro. Mechanism analysis indicated that NAP1L1 interacted with hepatoma-derived growth factor (HDGF) and they were co-localized in the cytoplasm. Furthermore, HDGF can interact with jun proto-oncogene (C-JUN), an oncogenic transformation factor that induces the expression of cyclin D1 (CCND1). Overexpressed HDGF in NAP1L1 knockdown OC cells not only increased the expression of C-JUN and CCND1, but it also reversed the suppressive effects of si-NAP1L1 on cell proliferation. Conclusions: Our data demonstrated that NAP1L1 could act as a prognostic biomarker in OC and can interact with HDGF to mediate the proliferation of OC, and this process of triggered proliferation may contribute to the activation of HDGF/C-JUN signaling in OC cells.
MeSH term(s)	Apoptosis/genetics ; Cell Line, Tumor ; Cell Proliferation ; Female ; Genes, jun ; Humans ; Intercellular Signaling Peptides and Proteins ; Nucleosome Assembly Protein 1/genetics ; Nucleosome Assembly Protein 1/metabolism ; Ovarian Neoplasms/pathology
Chemical Substances	Intercellular Signaling Peptides and Proteins ; NAP1L1 protein, human ; Nucleosome Assembly Protein 1 ; hepatoma-derived growth factor
Language	English
Publishing date	2022-03-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-022-09356-z
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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 ; 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 ; Online: Curcumin-Piperlongumine Hybrid Molecule Increases Cell Cycle Arrest and Apoptosis in Lung Cancer through JNK/c-Jun Signaling Pathway.

Zhang, Qianwen / Hui, Min / Chen, Guo / Huang, Huijing / Wang, Shiyu / Ye, Yanfei / Wang, Yan / Wang, Mengying / Zhang, Shuyuan / Huang, Lehao / Zhang, Fangjun / Liu, Zhiguo

Journal of agricultural and food chemistry

2024 Volume 72, Issue 13, Page(s) 7244–7255

Abstract: The instability of curcumin's structure and the toxic side effects of piperlongumine have limited their potential applications in cancer treatment. To overcome these challenges, we designed and synthesized a novel curcumin-piperlongumine hybrid molecule, ...

Abstract	The instability of curcumin's structure and the toxic side effects of piperlongumine have limited their potential applications in cancer treatment. To overcome these challenges, we designed and synthesized a novel curcumin-piperlongumine hybrid molecule, 3-[(
MeSH term(s)	Humans ; Curcumin/pharmacology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Cell Line, Tumor ; Cell Cycle Checkpoints ; Apoptosis ; Cell Proliferation ; MAP Kinase Signaling System ; Cell Cycle ; Benzodioxoles
Chemical Substances	Curcumin (IT942ZTH98) ; piperlonguminine (HN39MC8KIO) ; Benzodioxoles
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	241619-0
ISSN	1520-5118 ; 0021-8561
ISSN (online)	1520-5118
ISSN	0021-8561
DOI	10.1021/acs.jafc.4c00882
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Zs.A 1172: Show issues

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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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Zs.A 2109: 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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