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Article: A study related to the treatment of gastric cancer with Xiang-Sha-Liu-Jun-Zi-Tang based on network analysis.

Jiang, Ke / Liu, Heli / Ge, Jie / Yang, Bo / Wang, Yu / Wang, Wenbo / Wen, Yuqi / Zeng, Siqing / Chen, Quan / Huang, Jun / Xiong, Xingui

Heliyon

2023 Volume 9, Issue 9, Page(s) e19546

Abstract: Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer ...

Abstract	Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer(GC) and is widely used in clinical practice, however, there is a lack of investigation into its mechanism. Methods: We collected and organized drug and disease targets, constructed the "XSLJZT-Active Ingredient-Target" visualization network, and performed GO and KEGG functional enrichment analysis of crossover genes, followed by molecular docking of active ingredients and core targets. The best docked monomers were combined with weighted gene co-expression network analysis(WGCNA) and macroscopically analyzed by GO and KEGG enrichment techniques. The results of cluster gene difference analysis, ROC evaluation, and CIBERSORT immune infiltration analysis were evaluated and finally supported by cellular experiments. Results: The main components of XSLJZT are quercetin, stigmasterol, and naringenin, effectively treat GC by targeting STAT3, TP53 and MAPK3, which are involved in IL-17, TNF and HIF-1 signaling pathways. The results of molecular docking showed that quercetin bound better to the core targets. We performed an in-depth analysis of this monomer and found that quercetin acts on the core targets of TP53, MMP9, TIMP1 and MYC, and is involved in two key signaling pathways, TNF and IL-17, thus effectively treating GC. The experimental results are consistent with our analysis that quercetin inhibits the proliferation of GC cells and promotes apoptosis, and TP53, MYC and TIMP1 are the quercetin targets for the treatment of GC. Conclusion: The present study tentatively suggests that quercetin, the main active ingredient in XSLJZT, can exert a therapeutic effect on GC by targeting TIMP1.
Language	English
Publishing date	2023-08-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e19546
Database	MEDical Literature Analysis and Retrieval System OnLINE

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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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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: Molecular mechanism of methyl-dependent and spatial-specific DNA recognition of c-Jun homodimer.

Bie, Li-Hua / Fei, Jun-Wen / Gao, Jun

Journal of molecular modeling

2021 Volume 27, Issue 8, Page(s) 227

Abstract: ... By constructing four models of c-Jun/Jun protein binding to the 5[Formula: see text]-XGAGTCA-3[Formula: see text ...

Abstract	DNA methylation is important in regulation of gene expression and normal development because it alters the interplay between protein and DNA. Experiments have shown that a single 5-methylcytosine at different CpG sites (mCpG) might have different effects on specific recognition, but the atomistic origin and dynamic details are largely unclear. In this work, we investigated the mechanism of monomethylation at different CpG sites in the cognate motif and the cooperativity of full methylation. By constructing four models of c-Jun/Jun protein binding to the 5[Formula: see text]-XGAGTCA-3[Formula: see text] (X represents C or methylated C) motif, we characterized the dynamics of the contact interface using the all-atom molecular dynamics method. Free energy analysis of MM/GBSA suggests that regardless of whether the C12pG13 site of the bottom strand is methylated, the effects from mC25 of the top strand are dominant and can moderately enhance the binding by [Formula: see text] 31 kcal/mol, whereas mC12 showed a relatively small contribution, in agreement with the experimental data. Remarkably, we found that this spatial-specific influence was induced by different regulatory rules. The influence of the mC25 site is mainly mediated by steric hindrance. The additional methyl group leads to the conformational changes in nearby residues and triggers an obvious structural bending in the protein, which results in the formation of a new T-Asn-C triad that enhances the specific recognition of TCA half-sites. The substitution of the methyl group at the mC12 site of the bottom strand breaks the original H-bonds directly. Such changes in electrostatic interactions also lead to the remote allosteric effects of protein by multifaceted interactions but have negligible contributions to binding. Although these two influence modes are different, they can both fine-tune the local environment, which might produce remote allosteric effects through protein-protein interactions. Further analysis reveals that the discrepancies in these two modes are primarily due to their location. Moreover, when both sites are methylated, the major determinant of binding specificity depends on the context and the location of the methylation site, which is the result of crosstalk and cooperativity.
MeSH term(s)	Binding Sites/genetics ; CpG Islands/genetics ; DNA/genetics ; DNA Methylation/genetics ; DNA-Binding Proteins/genetics ; Dimerization ; JNK Mitogen-Activated Protein Kinases/chemistry ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/ultrastructure ; Molecular Dynamics Simulation ; Protein Binding/genetics
Chemical Substances	DNA-Binding Proteins ; DNA (9007-49-2) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-07-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1284729-X
ISSN	0948-5023 ; 1610-2940
ISSN (online)	0948-5023
ISSN	1610-2940
DOI	10.1007/s00894-021-04840-y
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Article ; Online: A study related to the treatment of gastric cancer with Xiang-Sha-Liu-Jun-Zi-Tang based on network analysis

Ke Jiang / Heli Liu / Jie Ge / Bo Yang / Yu Wang / Wenbo Wang / Yuqi Wen / Siqing Zeng / Quan Chen / Jun Huang / Xingui Xiong

Heliyon, Vol 9, Iss 9, Pp e19546- (2023)

2023

Abstract: Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer ...

Abstract	Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer(GC) and is widely used in clinical practice, however, there is a lack of investigation into its mechanism. Methods: We collected and organized drug and disease targets, constructed the “XSLJZT-Active Ingredient-Target” visualization network, and performed GO and KEGG functional enrichment analysis of crossover genes, followed by molecular docking of active ingredients and core targets. The best docked monomers were combined with weighted gene co-expression network analysis(WGCNA) and macroscopically analyzed by GO and KEGG enrichment techniques. The results of cluster gene difference analysis, ROC evaluation, and CIBERSORT immune infiltration analysis were evaluated and finally supported by cellular experiments. Results: The main components of XSLJZT are quercetin, stigmasterol, and naringenin, effectively treat GC by targeting STAT3, TP53 and MAPK3, which are involved in IL-17, TNF and HIF-1 signaling pathways. The results of molecular docking showed that quercetin bound better to the core targets. We performed an in-depth analysis of this monomer and found that quercetin acts on the core targets of TP53, MMP9, TIMP1 and MYC, and is involved in two key signaling pathways, TNF and IL-17, thus effectively treating GC. The experimental results are consistent with our analysis that quercetin inhibits the proliferation of GC cells and promotes apoptosis, and TP53, MYC and TIMP1 are the quercetin targets for the treatment of GC. Conclusion: The present study tentatively suggests that quercetin, the main active ingredient in XSLJZT, can exert a therapeutic effect on GC by targeting TIMP1.
Keywords	XSLJZT ; GC ; Network Pharmacology ; Molecular Docking ; WGCNA ; Mechanism of action ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
Subject code	004
Language	English
Publishing date	2023-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Development of a Covalent Inhibitor of c-Jun N-Terminal Protein Kinase (JNK) 2/3 with Selectivity over JNK1.

Journal of medicinal chemistry

2023 Volume 66, Issue 5, Page(s) 3356–3371

Abstract: The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK ...

Abstract	The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family, which includes JNK1-JNK3. Interestingly, JNK1 and JNK2 show opposing functions, with JNK2 activity favoring cell survival and JNK1 stimulating apoptosis. Isoform-selective small molecule inhibitors of JNK1 or JNK2 would be useful as pharmacological probes but have been difficult to develop due to the similarity of their ATP binding pockets. Here, we describe the discovery of a covalent inhibitor YL5084, the first such inhibitor that displays selectivity for JNK2 over JNK1. We demonstrated that YL5084 forms a covalent bond with Cys116 of JNK2, exhibits a 20-fold higher
MeSH term(s)	JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Phosphorylation
Chemical Substances	JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; YL5084
Language	English
Publishing date	2023-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.2c01834
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Article ; Online: KIAA1429 regulates cell proliferation by targeting c-Jun messenger RNA directly in gastric cancer.

Miao, Ran / Dai, Cong-Cong / Mei, Lin / Xu, Jun / Sun, Shan-Wen / Xing, Yun-Long / Wu, Li-Sheng / Wang, Ming-Hai / Wei, Ji-Fu

Journal of cellular physiology

2020 Volume 235, Issue 10, Page(s) 7420–7432

Abstract: ... targeted gene, c-Jun. We found that KIAA1429 was upregulated in gastric cancer tissues, and expressed lower ... regulating gene as c-Jun by mRNAs high-throughput sequencing and RIP assay. By luciferase assay, we verified ... that KIAA1429 regulated the expression of c-Jun in an m6A-independent manner. Finally, the overexpression of c ...

Abstract	N6-methyladenosine (m6A) modification regulatory proteins are involved in the development of many types of cancer. KIAA1429 serves as a scaffold in bridging the catalytic core components of the m6A methyltransferase complex. The role of KIAA1429 in gastric cancer and its related mechanism has not been reported upon. The expression of KIAA1429 was detected in human gastric cancer tissues and cell lines by quantitative real-time polymerase chain reaction and western blot. The effects of KIAA1429 on gastric cancer proliferation were evaluated by cell counting kit assays, colony formation assays, flow cytometry assay, and in vivo experiments with nude mice. And messenger RNA (mRNA) high-throughput sequencing, RNA immunoprecipitation assay (RIP), luciferase assay, and a rescue experiment were used to identify the relationship between KIAA1429 and its specific targeted gene, c-Jun. We found that KIAA1429 was upregulated in gastric cancer tissues, and expressed lower in adjacent tissues. The upregulated KIAA1429 promoted proliferation and downregulated KIAA1429 was proved to inhibit proliferation of gastric cancer in vitro and in vivo. Then, we identified the potential KIAA1429 regulating gene as c-Jun by mRNAs high-throughput sequencing and RIP assay. By luciferase assay, we verified that KIAA1429 regulated the expression of c-Jun in an m6A-independent manner. Finally, the overexpression of c-Jun rescued the inhibition of proliferation caused by KIAA1429 knockdown in gastric cancer cells. KIAA1429 could act as an oncogene in gastric cancer by stabilizing c-Jun mRNA in an m6A-independent manner. This highlights the functional role for KIAA1429 as a potential prognostic biomarker and therapeutic target in gastric cancer.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Down-Regulation/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Prognosis ; Proto-Oncogene Proteins c-jun/genetics ; RNA, Messenger/genetics ; RNA-Binding Proteins/genetics ; Stomach Neoplasms/genetics ; Stomach Neoplasms/pathology ; Up-Regulation/genetics ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Biomarkers, Tumor ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; RNA-Binding Proteins ; VIRMA protein, human
Language	English
Publishing date	2020-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.29645
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Article ; Online: MicroRNA-139-5p upregulation is associated with diabetic endothelial cell dysfunction by targeting c-jun.

Luo, Yu-Fang / Wan, Xin-Xing / Zhao, Li-Ling / Guo, Zi / Shen, Rui-Ting / Zeng, Ping-Yu / Wang, Ling-Hao / Yuan, Jing-Jing / Yang, Wen-Jun / Yue, Chun / Mo, Zhao-Hui

Aging

2020 Volume 13, Issue 1, Page(s) 1186–1211

Abstract: ... proliferation, and down-regulated expression of c-jun, vascular endothelial growth factor (VEGF), and ... of ECFCs by targeting c-jun-VEGF/PDGF-B pathway. ...

Abstract	Dysfunction of endothelial cells (ECs) and their progenitor cells is an important feature of diabetic vascular disease. MicroRNA (miR)-139-5p is involved in inhibiting the metastasis and progression of diverse malignancies. However, the role of miR-139-5p in ECs still remains unclarified. Here we demonstrated that miR-139-5p expression was elevated in endothelial colony-forming cells (ECFCs) isolated from patients with diabetes, ECs derived from the aorta of diabetic rodents, and human umbilical vein endothelial cells (HUVECs) cultured in high glucose media. MiR-139-5p mimics inhibited tube formation, migration, proliferation, and down-regulated expression of c-jun, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF)-B, in ECFCs and HUVECs, respectively; moreover, miR-139-5p inhibitors reversed the tendency. Further, gain- and-loss function experiments and ChIP assay indicated that miR-139-5p regulate functions of ECFCs by targeting c-jun-VEGF/PDGF-B pathway.
MeSH term(s)	Adult ; Animals ; Aorta/cytology ; Case-Control Studies ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Angiopathies/metabolism ; Endothelial Cells/metabolism ; Female ; Human Umbilical Vein Endothelial Cells ; Humans ; Male ; Mice ; MicroRNAs/metabolism ; Middle Aged ; Neovascularization, Physiologic/physiology ; Proto-Oncogene Proteins c-jun/metabolism ; Proto-Oncogene Proteins c-sis/metabolism ; Rats ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	MIRN139 microRNA, human ; MIRN139 microRNA, mouse ; MIRN139 microRNA, rat ; MicroRNAs ; Proto-Oncogene Proteins c-jun ; Proto-Oncogene Proteins c-sis ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2020-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.202257
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Article ; Online: Unraveling the Design and Discovery of c-Jun N-Terminal Kinase Inhibitors and Their Therapeutic Potential in Human Diseases.

Zhu, Yumeng / Shuai, Wen / Zhao, Min / Pan, Xiaoli / Pei, Junping / Wu, Yongya / Bu, Faqian / Wang, Aoxue / Ouyang, Liang / Wang, Guan

Journal of medicinal chemistry

2022 Volume 65, Issue 5, Page(s) 3758–3775

Abstract: c-Jun N-terminal kinases (JNKs), members of the mitogen-activated protein kinase (MAPK) family, are ...

Abstract	c-Jun N-terminal kinases (JNKs), members of the mitogen-activated protein kinase (MAPK) family, are encoded by three genes:
MeSH term(s)	Humans ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Neoplasms/drug therapy ; Phosphorylation ; Protein Isoforms/metabolism
Chemical Substances	Protein Isoforms ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.1c01947
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Article ; Online: IGFBP7 enhances trophoblast invasion via IGF-1R/c-Jun signaling in unexplained recurrent spontaneous abortion.

Wu, Pei-Li / Zhu, Jing-Wen / Zeng, Cheng / Li, Xin / Xue, Qing / Yang, Hui-Xia

Reproduction (Cambridge, England)

2022 Volume 164, Issue 5, Page(s) 231–241

Abstract: ... the level of c-Jun was significantly upregulated in the URSA group. Silencing IGFBP7 increased the binding ... of downstream c-Jun to the MMP2 and Slug promoter regions in HTR-8/SVneo cells, thus suppressing transcription ... that in normal pregnancy, IGFBP7 induces MMP2 and Slug expression via the IGF-1R-mediated c-Jun signaling pathway ...

Abstract	In brief: Insufficient trophoblast invasion at the maternal-fetal interface contributes to abortion-prone pregnancy. Our study shows that decreased levels of IGFBP7 in unexplained recurrent spontaneous abortion (URSA) trophoblast cells inhibit MMP2 and Slug expression as well as trophoblast invasion, suggesting that IGFBP7 should be considered a potential therapeutic protein target in URSA. Abstract: Insufficient trophoblast invasion at the maternal-fetal interface contributes to abortion-prone pregnancy. Cyclosporine A (CsA) can exert therapeutic effects on URSA by promoting trophoblast invasion. A previous study showed decreased expression of insulin-like growth factor-binding protein 7 (IGFBP7) in the sera of recurrent spontaneous abortion patients. However, the role of IGFBP7 in URSA remains unknown. The aim of this study was to determine whether IGFBP7 modulates trophoblast invasion in URSA and the underlying molecular mechanisms. We found that IGFBP7 was expressed at lower levels in villous specimens from URSA patients. Manipulating IGFBP7 expression significantly affected the MMP2 and Slug expression in HTR-8/SVneo cells as well as trophoblast invasion in vitro. Inactivation of IGF-1R by IGFBP7 was observed, and IGF-1R inhibition increased the IGFBP7-induced MMP2 and Slug expression in HTR-8/SVneo cells. Moreover, the level of c-Jun was significantly upregulated in the URSA group. Silencing IGFBP7 increased the binding of downstream c-Jun to the MMP2 and Slug promoter regions in HTR-8/SVneo cells, thus suppressing transcription. In addition, increased expression of IGFBP7 in HTR-8/SVneo cells was observed upon CsA treatment. Knockdown of IGFBP7 inhibited the CsA-enhanced MMP2 and Slug expression in HTR-8/SVneo cells. Our results suggest that in normal pregnancy, IGFBP7 induces MMP2 and Slug expression via the IGF-1R-mediated c-Jun signaling pathway, thereby promoting trophoblast invasion. IGFBP7 depletion in URSA inhibits MMP2 and Slug expression as well as trophoblast invasion. Moreover, IGFBP7 participates in CsA-induced trophoblast invasion, suggesting that IGFBP7 is a potential therapeutic target for URSA.
MeSH term(s)	Abortion, Habitual/metabolism ; Abortion, Spontaneous/metabolism ; Cell Movement ; Cyclosporine/pharmacology ; Female ; Humans ; Insulin-Like Growth Factor Binding Proteins/genetics ; Insulin-Like Growth Factor Binding Proteins/metabolism ; Matrix Metalloproteinase 2/genetics ; Matrix Metalloproteinase 2/metabolism ; Pregnancy ; Proto-Oncogene Proteins c-jun/metabolism ; Receptor, IGF Type 1/metabolism ; Signal Transduction ; Trophoblasts/metabolism
Chemical Substances	IGF1R protein, human ; Insulin-Like Growth Factor Binding Proteins ; Proto-Oncogene Proteins c-jun ; insulin-like growth factor binding protein-related protein 1 ; Cyclosporine (83HN0GTJ6D) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; Matrix Metalloproteinase 2 (EC 3.4.24.24)
Language	English
Publishing date	2022-10-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2034501-X
ISSN	1741-7899 ; 1470-1626 ; 1476-3990
ISSN (online)	1741-7899
ISSN	1470-1626 ; 1476-3990
DOI	10.1530/REP-21-0501
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