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Article ; Online: Notch-mediated lactate metabolism regulates MDSC development through the Hes1/MCT2/c-Jun axis.

Zhao, Jun-Long / Ye, Yu-Chen / Gao, Chun-Chen / Wang, Liang / Ren, Kai-Xi / Jiang, Ru / Hu, Si-Jun / Liang, Shi-Qian / Bai, Jian / Liang, Jia-Long / Ma, Peng-Fei / Hu, Yi-Yang / Li, Ben-Chang / Nie, Yong-Zhan / Chen, Yan / Li, Xiao-Fei / Zhang, Wei / Han, Hua / Qin, Hong-Yan

Cell reports

2022 Volume 38, Issue 10, Page(s) 110451

Abstract: ... Jun as a novel intracellular sensor of lactate in myeloid cells using liquid-chromatography ... mass spectrometry (LC-MS) followed by CRISPR-Cas9-mediated gene disruption. Meanwhile, lactate interacts with c-Jun ... between the Notch-MCT2/lactate-c-Jun axis in myeloid cells and tumorigenesis is also confirmed in clinical ...

Abstract	Myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) play critical roles in tumorigenesis. However, the mechanisms underlying MDSC and TAM development and function remain unclear. In this study, we find that myeloid-specific activation of Notch/RBP-J signaling downregulates lactate transporter MCT2 transcription via its downstream molecule Hes1, leading to reduced intracellular lactate levels, blunted granulocytic MDSC (G-MDSC) differentiation, and enhanced TAM maturation. We identify c-Jun as a novel intracellular sensor of lactate in myeloid cells using liquid-chromatography-mass spectrometry (LC-MS) followed by CRISPR-Cas9-mediated gene disruption. Meanwhile, lactate interacts with c-Jun to protect from FBW7 ubiquitin-ligase-mediated degradation. Activation of Notch signaling and blockade of lactate import repress tumor progression by remodeling myeloid development. Consistently, the relationship between the Notch-MCT2/lactate-c-Jun axis in myeloid cells and tumorigenesis is also confirmed in clinical lung cancer biopsies. Taken together, our current study shows that lactate metabolism regulated by activated Notch signaling might participate in MDSC differentiation and TAM maturation.
MeSH term(s)	Carcinogenesis/genetics ; Humans ; Lactic Acid ; Myeloid Cells ; Myeloid-Derived Suppressor Cells ; Signal Transduction ; Transcription Factor HES-1
Chemical Substances	Transcription Factor HES-1 ; HES1 protein, human (149348-15-2) ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2022-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110451
Database	MEDical Literature Analysis and Retrieval System OnLINE

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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: 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 ; Online: Knockdown of AK142426 suppresses M2 macrophage polarization and inflammation in peritoneal fibrosis via binding to c-Jun.

Shao, Qiuyuan / Jiang, Chunming / Zhang, Qingyan / Liu, Jing / Jin, Bo / Zhao, Min / Xia, Yangyang

The journal of gene medicine

2023 Volume 25, Issue 9, Page(s) e3524

Abstract: ... measured by ELISA assay. The direct interaction between AK142426 and c-Jun was evaluated by RNA pull-down ... assay. In addition, the c-Jun and fibrosis related proteins were assessed by western blot analysis ... AK142426 could upregulate c-Jun through binding c-Jun protein. In rescue experiments, overexpression of c ...

Abstract	Background: Peritoneal fibrosis is a common complication of peritoneal dialysis, which may lead to ultrafiltration failure and ultimately treatment discontinuation. LncRNAs participate in many biological processes during tumorigenesis. We investigated the role of AK142426 in peritoneal fibrosis. Methods: The AK142426 level in peritoneal dialysis (PD) fluid was detected by quantitative real-time-PCR assay. The M2 macrophage distribution was determined by flow cytometry. The inflammatory cytokines of TNF-α and TGF-β1 were measured by ELISA assay. The direct interaction between AK142426 and c-Jun was evaluated by RNA pull-down assay. In addition, the c-Jun and fibrosis related proteins were assessed by western blot analysis. Results: The PD-induced peritoneal fibrosis mouse model was successfully established. More importantly, PD treatment induced M2 macrophage polarization and the inflammation in PD fluid, which might be associated with exosome transmission. Fortunately, AK142426 was observed to be upregulated in PD fluid. Mechanically, knockdown of AK142426 suppressed M2 macrophage polarization and inflammation. Furthermore, AK142426 could upregulate c-Jun through binding c-Jun protein. In rescue experiments, overexpression of c-Jun could partially abolish the inhibitory effect of sh-AK142426 on the activation of M2 macrophages and inflammation. Consistently, knockdown of AK142426 alleviated peritoneal fibrosis in vivo. Conclusions: This study demonstrated that knockdown of AK142426 suppressed M2 macrophage polarization and inflammation in peritoneal fibrosis via binding to c-Jun, suggesting that AK142426 might be a promising therapeutic target for patients of peritoneal fibrosis.
MeSH term(s)	Animals ; Mice ; Dialysis Solutions/metabolism ; Dialysis Solutions/pharmacology ; Inflammation/genetics ; Macrophages/metabolism ; Macrophages/pathology ; Peritoneal Dialysis/adverse effects ; Peritoneal Fibrosis/genetics ; Peritoneal Fibrosis/metabolism
Chemical Substances	Dialysis Solutions ; Actb protein, mouse
Language	English
Publishing date	2023-05-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1458024-x
ISSN	1521-2254 ; 1099-498X
ISSN (online)	1521-2254
ISSN	1099-498X
DOI	10.1002/jgm.3524
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Zs.A 5423: Show issues

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Article ; Online: SENP3-mediated deSUMOylation of c-Jun facilitates microglia-induced neuroinflammation after cerebral ischemia and reperfusion injury.

Xia, Qian / Mao, Meng / Zhan, Gaofeng / Luo, Zhenzhao / Zhao, Yin / Li, Xing

iScience

2023 Volume 26, Issue 6, Page(s) 106953

Abstract: ... in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun ... by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 ... expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic ...

Abstract	Recent evidences have implicated that SENP3 is a deSUMOylase which possesses neuronal damage effects in cerebral ischemia. However, its role in microglia remains poorly understood. Here, we found that SENP3 was upregulated in the peri-infarct areas of mice following ischemic stroke. Furthermore, knockdown of SENP3 significantly inhibits the expression of proinflammatory cytokines and chemokines in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun, which activated its transcriptional activity, ultimately followed by the activation of MAPK/AP-1 signaling pathway. In addition, microglia-specific SENP3 knockdown alleviated ischemia-induced neuronal damage, and markedly diminished infract volume, ameliorated sensorimotor and cognitive function in animals subjected to ischemic stroke. These results indicated SENP3 functions as a novel regulator of microglia-induced neuroinflammation by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic stroke.
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106953
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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: Analysis of the Promoter Regions of gga-miR-31 and Its Regulation by RA and C-jun in Chicken.

Wang, Yingjie / Kong, Ruihong / Xie, Ke / Hu, Cai / Zhao, Zongyi / Wu, Yuhui / Zuo, Qisheng / Li, Bichun / Zhang, Yani

International journal of molecular sciences

2023 Volume 24, Issue 15

Abstract: ... promoter regions was found to be competitive. Through the deletion of C-jun binding sites and the manipulation of C ... jun expression levels, it was determined that C-jun inhibits the activity of the gga-miR-31 promoter ... Furthermore, the combined treatment of C-jun and RA demonstrated that the positive regulatory effect of RA ...

Abstract	The role of gga-miR-31 in chicken germ cell differentiation and spermatogenesis is of significant importance. The transcriptional properties of gga-miR-31 are crucial in establishing the foundation for the formation of chicken spermatogonia stem cells and spermatogenesis. In this study, a series of recombinant vectors including varying lengths of the gga-miR-31 promoter were predicted and constructed. Through the utilization of the dual luciferase reporting system, the upstream -2180~0 bp region of gga-miR-31 was identified as its promoter region. Furthermore, it was predicted and confirmed that the activity of the gga-miR-31 promoter is increased by retinoic acid (RA). The binding of RA to the gga-miR-31 and Stra8 promoter regions was found to be competitive. Through the deletion of C-jun binding sites and the manipulation of C-jun expression levels, it was determined that C-jun inhibits the activity of the gga-miR-31 promoter. Furthermore, the combined treatment of C-jun and RA demonstrated that the positive regulatory effect of RA on the gga-miR-31 promoter is attenuated in the presence of high levels of C-jun. Overall, this study establishes a foundation for further investigation into the regulatory mechanisms of gga-miR-31 action, and provides a new avenue for inducing chicken embryonic stem cells (ESC) to differentiate into spermatogonial stem cells (SSC), and sperm formation.
MeSH term(s)	Chick Embryo ; Animals ; Male ; Tretinoin/pharmacology ; Chickens/genetics ; Chickens/metabolism ; Semen/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Promoter Regions, Genetic
Chemical Substances	Tretinoin (5688UTC01R) ; MicroRNAs
Language	English
Publishing date	2023-08-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241512516
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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: NR0B1 suppresses ferroptosis through upregulation of NRF2/c-JUN-CBS signaling pathway in lung cancer cells.

Zhang, Xin-Yue / Zhang, Hao / Hu, Si-Jing / Liao, Shun-Yao / Tao, Da-Chang / Tan, Xiao-Lan / Yi, Ming / Leng, Xiang-You / Wang, Zhao-Kun / Shi, Jia-Ying / Xie, Sheng-Yu / Yang, Yuan / Liu, Yun-Qiang

American journal of cancer research

2023 Volume 13, Issue 11, Page(s) 5174–5196

Abstract: ... and the expression level of NR0B1 positively correlated with that of c-JUN, NRF2, and CBS. We further ... revealed that NR0B1 suppression of ferroptosis depended on the activities of c-JUN, NRF2, and CBS. NR0B1 ... directly promoted the expression of NRF2 and c-JUN and indirectly upregulated CBS expression ...

Abstract	Ferroptosis has demonstrated significant potential in treating radiochemotherapy-resistant cancers, but its efficacy can be affected by recently discovered ferroptosis suppressors. In this study, we discovered that NR0B1 protects against erastin- or RSL3-induced ferroptosis in lung cancer cells. Transcriptomic analysis revealed that NR0B1 significantly interfered with the expression of 12 ferroptosis-related genes, and the expression level of NR0B1 positively correlated with that of c-JUN, NRF2, and CBS. We further revealed that NR0B1 suppression of ferroptosis depended on the activities of c-JUN, NRF2, and CBS. NR0B1 directly promoted the expression of NRF2 and c-JUN and indirectly upregulated CBS expression through enhancing NRF2 and/or c-JUN transcription. Moreover, we showed that NR0B1 depletion restrained xenograft tumor growth and facilitated RSL3-induced ferroptosis in the tumors. In conclusion, our findings uncover that NR0B1 suppresses ferroptosis by activating the c-JUN/NRF2-CBS signaling pathway in lung cancer cells, providing new evidence for the involvement of NR0B1 in drug resistance during cancer therapy.
Language	English
Publishing date	2023-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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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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