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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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: USP5 facilitates bladder cancer progression by stabilizing the c-Jun protein.

Zhang, Hui-Hui / Zhang, An-Qi / Peng, Peng / Huang, Liang / Liu, Cai-Ying / Nie, Xin-Rui / Hou, De-Fu / Zhang, Xia / Li, Shang-Ze

Cancer cell international

2024 Volume 24, Issue 1, Page(s) 32

Abstract: ... and c-Jun. Cycloheximide (CHX) chase assays were performed to establish the effect of USP5 on c-Jun ... USP5 and c-Jun. USP5 was found to activate c-Jun by inhibiting its ubiquitination.: Conclusions ... Our results show that high USP5 expression promotes bladder cancer progression by stabilizing c-Jun and ...

Abstract	Background: Bladder cancer is the second most common genitourinary malignancy worldwide. The death rate of bladder cancer has increased every year. However, the molecular mechanism of bladder cancer is not sufficiently studied. Deubiquitinating enzymes (DUBs) play an important role in carcinogenesis. Several studies have demonstrated that USP5 associated with malignancy and pathological progression in hepatocellular carcinoma, colorectal and non-small cell lung cancer. However, the role of USP5 in bladder cancer need to be explored. Methods: The USP5 expression was analysed using the web server GEPIA. To explore USP5 function in bladder cancer, we constructed USP5-knockout cell lines in T24 cells. A FLAG-USP5 (WT USP5) plasmid and a plasmid FLAG-USP5 C335A (catalytic-inactive mutant) used to overexpress USP5 in EJ cells. CCK8, colony formation, transwell and scratch assays were used to assess cell viability, proliferation and migration. RNA sequencing (RNA-seq) and dual-luciferase reporter assays were performed to screen the pathway. Coimmunoprecipitation and immunofluorescence were used to explore the interaction between USP5 and c-Jun. Cycloheximide (CHX) chase assays were performed to establish the effect of USP5 on c-Jun stability. Xenograft mouse model was used to study the role of USP5 in bladder cancer. Results: USP5 expression is increased in bladder cancer patients. Genetic ablation of USP5 markedly inhibited bladder cancer cell proliferation, viability, and migration both in vitro and in vivo. RNA-seq and luciferase pathway screening showed that USP5 activated JNK signalling, and we identified the interaction between USP5 and c-Jun. USP5 was found to activate c-Jun by inhibiting its ubiquitination. Conclusions: Our results show that high USP5 expression promotes bladder cancer progression by stabilizing c-Jun and that USP5 is a potential therapeutic target in bladder cancer.
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-024-03222-7
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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: 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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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: c-JUN-mediated transcriptional responses in lymphatic endothelial cells are required for lung fluid clearance at birth.

Fu, Siling / Wang, Yanxiao / Bin, Ennan / Huang, Huanwei / Wang, Fengchao / Tang, Nan

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 2, Page(s) e2215449120

Abstract: ... We identified that the expression of c-JUN is transiently upregulated in P0 LECs. Conditional knockout of ...

Abstract	Fluid clearance mediated by lymphatic vessels is known to be essential for lung inflation and gas-exchange function during the transition from prenatal to postnatal life, yet the molecular mechanisms that regulate lymphatic function remain unclear. Here, we profiled the molecular features of lymphatic endothelial cells (LECs) in embryonic and postnatal day (P) 0 lungs by single-cell RNA-sequencing analysis. We identified that the expression of c-JUN is transiently upregulated in P0 LECs. Conditional knockout of
MeSH term(s)	Humans ; Infant, Newborn ; Endothelial Cells/metabolism ; Lung/metabolism ; Lymphatic Vessels/metabolism
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2215449120
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Article ; Online: ANKRD49 promotes the metastasis of NSCLC via activating JNK-ATF2/c-Jun-MMP-2/9 axis.

Sun, Jia / Hu, Jin-Rui / Liu, Chao-Feng / Li, Yuan / Wang, Wei / Fu, Rong / Guo, Min / Wang, Hai-Long / Pang, Min

BMC cancer

2023 Volume 23, Issue 1, Page(s) 1108

Abstract: ... performed to in vitro. Immunoprecipitation was performed to test the interaction of c-Jun and ATF2 ... Chromatin immunoprecipitation was conducted to assess the transcriptional regulation of ATF2/c-Jun on MMP-2/9. Moreover ... phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2 ...

Abstract	Background: Ankyrin repeat domain 49 (ANKRD49) has been found to be highly expressed in multiple cancer including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). However, the function of ANKRD49 in the pathogenesis of NSCLC still remains elusive. Previously, ANKRD49 has been demonstrated to promote the invasion and metastasis of A549 cells, a LUAD cell line, via activating the p38-ATF-2-MMP2/MMP9 pathways. Considering the heterogeneity of tumor cells, the function and mechanism of ANKRD49 in NSCLC need more NSCLC-originated cells to clarify. Methods: Real-time qPCR was employed to test ANKRD49 expression levels in nine pairs of fresh NSCLC tissues and the corresponding adjacent normal tissues. The function of ANKRD49 was investigated using overexpression and RNA interference assays in lung adenocarcinoma cell line (NCI-H1299) and lung squamous carcinoma cell line (NCI-H1703) through gelatin zymography, cell counting kit-8, colony formation, wound healing, migration and invasion assays mmunoprecipitation was performed to in vitro. Immunoprecipitation was performed to test the interaction of c-Jun and ATF2. Chromatin immunoprecipitation was conducted to assess the transcriptional regulation of ATF2/c-Jun on MMP-2/9. Moreover, the tumorigenicity of ANKRD49 was evaluated in nude mice models and the involved signal molecular was also measured by immunohistochemical method. Results: We found that the levels of ANKRD49 in cancerous tissues were higher than those in adjacent normal tissues. in vitro assay showed that ANKRD49 promoted the migration and invasion of NCI-H1299 and NCI-H1703 cells via enhancing the levels of MMP-2 and MMP-9. Furthermore, ANKRD49 elevated phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2:c-Jun with the promoter MMP-2 or MMP-9. In vivo assay showed that ANKRD49 promoted lung metastasis of injected-NSCLC cells and the high metastatic rate was positively correlated with the high expression of ANKRD49, MMP-2, MMP-9, p-JNK, p-c-Jun and p-ATF2. Conclusion: The present study indicated that ANKRD49 accelerated the invasion and metastasis of NSCLC cells via JNK-mediated transcription activation of c-Jun and ATF2 which regulated the expression of MMP-2/MMP-9. The molecular mechanisms of ANKRD49's function is different from those found in A549 cells. The current study is a supplement and improvement to the previous research.
MeSH term(s)	Animals ; Mice ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice, Nude ; Cell Proliferation/genetics ; Cell Line, Tumor ; Carcinoma, Non-Small-Cell Lung/pathology ; Lung Neoplasms/pathology ; Carcinoma, Squamous Cell ; Adenocarcinoma of Lung
Chemical Substances	Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2023-11-14
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/s12885-023-11612-9
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Article ; Online: Remote regulation of rs80245547 and rs72673891 mediated by transcription factors C-Jun and CREB1 affect

Li, Jin-Xiu / Huang, Xue-Zhen / Fu, Wei-Ping / Zhang, Xiao-Hua / Mauki, David H / Zhang, Jing / Sun, Chang / Dai, Lu-Ming / Zhong, Li / Yu, Li / Zhang, Ya-Ping

iScience

2023 Volume 26, Issue 8, Page(s) 107383

Abstract: Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, is influenced by genetic factors. The genetic signal rs10516526 in the glutathione S-transferase C-terminal domain containing ( ...

Abstract	Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, is influenced by genetic factors. The genetic signal rs10516526 in the glutathione S-transferase C-terminal domain containing (
Language	English
Publishing date	2023-07-31
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.107383
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Article: Targeting c-Jun in A549 Cancer Cells Exhibits Antiangiogenic Activity

Shao, Chen / Huang, Yingying / Fu, Bingjie / Pan, Shunli / Zhao, Xiaoxia / Zhang, Ning / Wang, Wei / Zhang, Zhe / Qiu, Yuling / Wang, Ran / Jin, Meihua / Kong, Dexin

Frontiers in oncology

2021 Volume 11, Page(s) 663183

Abstract: The oncogene c-Jun is activated by Jun N-terminal kinase (JNK). Exosomes are nanometer-sized ... By using specific JNK inhibitor SP600125 or CRISPR/Cas9 to delete c-Jun, we found that exosomes ... from SP600125-treated A549 cancer cells (Exo-SP) or from c-Jun-KO-A549 cells (Exo-c-Jun-KO) dramatically ...

Abstract	The oncogene c-Jun is activated by Jun N-terminal kinase (JNK). Exosomes are nanometer-sized membrane vesicles released from a variety of cell types, and are essential for cell-to-cell communication. By using specific JNK inhibitor SP600125 or CRISPR/Cas9 to delete c-Jun, we found that exosomes from SP600125-treated A549 cancer cells (Exo-SP) or from c-Jun-KO-A549 cells (Exo-c-Jun-KO) dramatically inhibited tube formation of HUVECs. And the miR-494 levels in SP600125 treated or c-Jun-KO A549 cells, Exo-SP or Exo-c-Jun-KO, and HUVECs treated with Exo-SP or Exo-c-Jun-KO were significantly decreased. Meanwhile, Exo-SP and Exo-c-Jun-KO enhanced expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Addition of miR-494 agomir in Exo-c-Jun-KO treated HUVECs inhibited PTEN expression and promoted tube formation, suggesting the target of miR-494 might be PTEN in HUVECs. Moreover, A549 tumor xenograft model and Matrigel plug assay demonstrated that Exo-c-Jun-KO attenuated tumor growth and angiogenesis through reducing miR-494. Taken together, inhibition of c-Jun in A549 cancer cells exhibited antiangiogenic activity
Language	English
Publishing date	2021-04-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.663183
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