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  1. Article: Qizhu Anti-Cancer Recipe promotes anoikis of hepatocellular carcinoma cells by activating the c-Jun N-terminal kinase pathway.

    Han, Zhiyi / Huang, Qi / Lv, Minling / Ma, Mengqing / Zhang, Wei / Feng, Wenxing / Hu, Rui / Sun, Xinfeng / Li, Jing / Zhong, Xin / Zhou, Xiaozhou

    Heliyon

    2023  Volume 9, Issue 11, Page(s) e22089

    Abstract: Background: Qizhu Anti-Cancer Recipe (QACR) is a traditional Chinese medicine widely used in treating several liver diseases. However, its function and the relevant mechanism underlying its effect in treating hepatocellular carcinoma (HCC) remain ... ...

    Abstract Background: Qizhu Anti-Cancer Recipe (QACR) is a traditional Chinese medicine widely used in treating several liver diseases. However, its function and the relevant mechanism underlying its effect in treating hepatocellular carcinoma (HCC) remain unknown. The aim of this study was to explore the effect of QACR in HCC, which are expected to be a potential therapeutic scheme for HCC.
    Materials and methods: The chemical compositions of QACR were determined by liquid chromatography/quadrupole time-of-fight mass spectrometry (LC-QTOF-MS). The anoikis-resistant HCC cell proliferation and angiopoiesis were detected using the cell counting kit 8 (CCK8) assay, trypan blue, calcein AM/EthD-1, flow cytometer, Western blot, and tube formation assays. An orthotopic xenograft mouse model was established to evaluate the
    Results: QACR reduced the growth and tube formation of anoikis-resistant HCC cells and enhanced cell apoptosis
    Conclusion: Our study suggests that QACR suppresses the proliferation and angiopoiesis of anoikis-resistant HCC cells by activating the JNK pathway. Therefore, QACR is a promising new therapeutic strategy for treating hepatocellular carcinoma.
    Language English
    Publishing date 2023-11-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2023.e22089
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Thinkful of Icariin Induces Triple-Negative Breast Cancer Cell Apoptosis and Suppresses Invasion by Inhibiting the JNK/c-Jun Signaling Pathway [Response to Letter].

    Gao, Shenghan / Zhang, Xinyu / Liu, Jie / Lv, Yonggang / Shi, Wenzhen

    Drug design, development and therapy

    2023  Volume 17, Page(s) 1611–1612

    MeSH term(s) Humans ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; MAP Kinase Signaling System ; Cell Line, Tumor ; Apoptosis
    Chemical Substances icariin (VNM47R2QSQ)
    Language English
    Publishing date 2023-05-29
    Publishing country New Zealand
    Document type Letter ; Comment
    ZDB-ID 2451346-5
    ISSN 1177-8881 ; 1177-8881
    ISSN (online) 1177-8881
    ISSN 1177-8881
    DOI 10.2147/DDDT.S418906
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Icariin Induces Triple-Negative Breast Cancer Cell Apoptosis and Suppresses Invasion by Inhibiting the JNK/c-Jun Signaling Pathway.

    Gao, Shenghan / Zhang, Xinyu / Liu, Jie / Ji, Fuqing / Zhang, Zhihao / Meng, Qingjie / Zhang, Qi / Han, Xiaogang / Wu, He / Yin, Yulong / Lv, Yonggang / Shi, Wenzhen

    Drug design, development and therapy

    2023  Volume 17, Page(s) 821–836

    Abstract: ... signaling pathway. ICA treatment inhibited the expression of JNK and c-Jun and downregulated the antiapoptotic gene ... of ROS in cells and suppress TNBC cell invasion via the JNK/c-Jun signaling pathway.: Conclusion ... In addition, ICA could inhibit TNBC cell invasion through the JNK/c-Jun signaling pathway. The above suggests ...

    Abstract Background: Breast cancer is a common cancer worldwide. Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer characterized by a poor prognosis. Icariin (ICA) is a flavonoid glycoside purified from the natural product Epimedium, which is reported to exert an inhibitory effect on a variety of cancers. However, molecular mechanisms behind ICA suppressed TNBC remain elusive.
    Methods: The curative effects of ICA on TNBC cells and potential targets were predicted by network pharmacology and molecular biology methods screening, and the mechanism of inhibition was explained through in vitro experiments such as cell function determination, Western blot analysis, molecular docking verification, etc.
    Results: This study showed that ICA inhibits TNBC cell functions such as proliferation, migration, and invasion in a dose-dependent manner. ICA could induce redox-induced apoptosis in TNBC cell, as shown by ROS upregulation. As a result of network pharmacology, ICA was predicted to be able to inhibit the MAPK signaling pathway. ICA treatment inhibited the expression of JNK and c-Jun and downregulated the antiapoptotic gene cIAP-2. Our results suggested that ICA could induce apoptosis by inducing an excessive accumulation of ROS in cells and suppress TNBC cell invasion via the JNK/c-Jun signaling pathway.
    Conclusion: We demonstrated that ICA can effectively inhibit cell proliferation and induced apoptosis of TNBC cells. In addition, ICA could inhibit TNBC cell invasion through the JNK/c-Jun signaling pathway. The above suggests that ICA may become a potential drug for TNBC.
    MeSH term(s) Humans ; Cell Line, Tumor ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Reactive Oxygen Species/metabolism ; Molecular Docking Simulation ; Signal Transduction ; Cell Proliferation ; Apoptosis ; Cell Movement
    Chemical Substances icariin (VNM47R2QSQ) ; Reactive Oxygen Species
    Language English
    Publishing date 2023-03-20
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2451346-5
    ISSN 1177-8881 ; 1177-8881
    ISSN (online) 1177-8881
    ISSN 1177-8881
    DOI 10.2147/DDDT.S398887
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: JUN activation modulates chromatin accessibility to drive TNFα-induced mesenchymal transition in glioblastoma.

    Lv, Xuejiao / Li, Qian / Liu, Hang / Gong, Meihan / Zhao, Yingying / Hu, Jinyang / Wu, Fan / Wu, Xudong

    Journal of cellular and molecular medicine

    2022  Volume 26, Issue 16, Page(s) 4602–4612

    Abstract: ... we profile the chromatin accessibility dynamics during mesenchymal transition. Moreover, we identify the JUN ... Accordingly, inhibition of JUN phosphorylation and therefore its transcription activity successfully impedes ... on experimental models, JUN activity is positively correlated with mesenchymal features in clinical glioblastoma ...

    Abstract Chromatin dynamics as well as genetic evolution underlies the adaptability of tumour cells to environmental cues. Three subtypes of tumour cells have been identified in glioblastoma, one of the commonest malignant brain tumours in adults. During tumour progression or under therapeutic pressure, the non-mesenchymal subtypes may progress to the mesenchymal subtype, leading to unfavourable prognosis. However, the molecular mechanisms for this transition remain poorly understood. Here taking a TNFα-induced cellular model, we profile the chromatin accessibility dynamics during mesenchymal transition. Moreover, we identify the JUN family as one of the key driving transcription factors for the gained chromatin accessibility. Accordingly, inhibition of JUN phosphorylation and therefore its transcription activity successfully impedes TNFα-induced chromatin remodelling and mesenchymal transition. In line with these findings based on experimental models, JUN activity is positively correlated with mesenchymal features in clinical glioblastoma specimens. Together, this study unveils a deregulated transcription regulatory network in glioblastoma progression and hopefully provides a rationale for anti-glioblastoma therapy.
    MeSH term(s) Adult ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Chromatin/genetics ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Proto-Oncogene Proteins c-jun ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/pharmacology
    Chemical Substances Chromatin ; Proto-Oncogene Proteins c-jun ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2022-07-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.17490
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5752: Show issues Location:
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  5. Article ; Online: Quantitative Proteomics Based on iTRAQ Reveal that Nitidine Chloride Induces Apoptosis by Activating JNK/c-Jun Signaling in Hepatocellular Carcinoma Cells.

    Chen, Shipeng / Liao, Yinan / Lv, Jinyan / Hou, Huaxin / Feng, Jie

    Planta medica

    2022  Volume 88, Issue 13, Page(s) 1233–1244

    Abstract: The aim of the present study was to investigate the cytotoxic effects and underlying molecular mechanisms of nitidine chloride (NC) in hepatocellular carcinoma cells via quantitative proteomics. MTT assays were used to detect the inhibitory effects of NC ...

    Abstract The aim of the present study was to investigate the cytotoxic effects and underlying molecular mechanisms of nitidine chloride (NC) in hepatocellular carcinoma cells via quantitative proteomics. MTT assays were used to detect the inhibitory effects of NC in Bel-7402 liver cancer cells, and the number of apoptotic cells was measured by flow cytometry. Quantitative proteomics technology based on iTRAQ was used to discover differential expressed proteins after NC treatment, and bioinformatic techniques were further used to screen potential targets of NC. Molecular docking was applied to evaluate the docking activity of NC with possible upstream proteins, and their expression was detected at the mRNA and protein levels by quantitative reverse transcription PCR and western blotting. NC inhibited the proliferation of Bel-7402 cells after 24 h of treatment and stimulated apoptosis
    MeSH term(s) Carcinoma, Hepatocellular/drug therapy ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Transcription Factor AP-1/metabolism ; Proteomics ; Molecular Docking Simulation ; Cell Line, Tumor ; Apoptosis ; JNK Mitogen-Activated Protein Kinases/metabolism ; RNA, Messenger
    Chemical Substances nitidine (933301178Z) ; Transcription Factor AP-1 ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; RNA, Messenger
    Language English
    Publishing date 2022-02-01
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 123545-x
    ISSN 1439-0221 ; 0032-0943
    ISSN (online) 1439-0221
    ISSN 0032-0943
    DOI 10.1055/a-1676-4307
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uf I Zs.157: Show issues Location:
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  6. Article ; Online: Nobiletin inhibits breast cancer cell migration and invasion by suppressing the IL-6-induced ERK-STAT and JNK-c-JUN pathways.

    Wu, Yuan / Li, Qiong / Lv, Ling-Ling / Chen, Jing-Xian / Ying, Hai-Feng / Ruan, Ming / Zhu, Wen-Hua / Xu, Jia-Yue / Zhang, Chen-Yiyu / Zhang, Kai-Yuan / Guo, Yuan-Biao / Zhu, Wei-Rong / Zheng, Lan

    Phytomedicine : international journal of phytotherapy and phytopharmacology

    2022  Volume 110, Page(s) 154610

    Abstract: ... of extracellular signal-regulated kinases (ERK) and the c-Jun N-terminal kinase (JNK) signalling pathways. Molecular docking was used ... Nobiletin inhibited liver metastasis of breast cancer by downregulating the ERK-STAT and JNK-c-JUN pathways ...

    Abstract Background: Breast cancer is one of the most common cancers in women, affecting more than 2 million women worldwide annually. However, effective treatments for breast cancer are limited. Nobiletin is a flavonoid present in the dried mature pericarp of mandarin orange (Citrus reticulata Blanco), which is used to prepare Citri Renetulatae Pericarpium and can inhibit tumour growth and progression according to modern pharmacological studies. However, whether nobiletin exhibits an antimetastatic role in breast cancer and its potential mechanism need to be further investigated.
    Purpose: This study aims to evaluate the inhibitory effect of nobiletin on breast cancer and to elucidate potential mechanisms against invasion and migration.
    Methods: Cell viability was determined by cell counting kit-8 and colony formation assays. Wound healing and Boyden chamber assays detected cancer cell migration and invasion capabilities. Immunoblotting and qPCR were applied to determine the protein and mRNA expression levels of extracellular signal-regulated kinases (ERK) and the c-Jun N-terminal kinase (JNK) signalling pathways. Molecular docking was used to assess the degree of nobiletin binding to phosphatidylinositol 3-kinase (PI3K). Xenografts and liver metastases were constructed in BALB/c nude mice to evaluate the anticancer effect of nobiletin in vivo. H&E staining and immunohistochemistry were used to detect proliferation and the expression of related proteins.
    Results: Nobiletin induced cell death in a concentration- and time-dependent manner and possessed anti-invasion and anti-migration effects on MCF-7 and T47D cells by suppressing the interleukin-6-induced ERK and JNK signalling pathways. In addition, nobiletin docked with the binding site of PI3K, and the binding score was -8.0 kcal/mol. Furthermore, the inhibition of breast cancer growth and metastasis by nobiletin was demonstrated by constructing xenografts and liver metastases in vivo.
    Conclusion: Nobiletin inhibited liver metastasis of breast cancer by downregulating the ERK-STAT and JNK-c-JUN pathways, and its safety and efficacy were verified, indicating the potential of nobiletin as an anticancer agent.
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Interleukin-6/pharmacology ; Liver Neoplasms ; Mice, Nude ; Molecular Docking Simulation ; Phosphatidylinositol 3-Kinases/metabolism
    Chemical Substances Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Interleukin-6 ; nobiletin (D65ILJ7WLY) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; IL6 protein, human ; JUN protein, human
    Language English
    Publishing date 2022-12-17
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1205240-1
    ISSN 1618-095X ; 0944-7113
    ISSN (online) 1618-095X
    ISSN 0944-7113
    DOI 10.1016/j.phymed.2022.154610
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4115: Show issues Location:
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  7. Article ; Online: Promotion Effect of EGCG on the Raised Expression of IL-23 through the Signaling of STAT3-BATF2-c-JUN/ATF2.

    Hu, Yaozhong / Gu, Jiaxin / Wang, Yi / Lin, Jing / Yu, Huaning / Yang, Feier / Wu, Sihao / Yin, Jia / Lv, Huan / Ji, Xuemeng / Wang, Shuo

    Journal of agricultural and food chemistry

    2021  Volume 69, Issue 28, Page(s) 7898–7909

    Abstract: ... which could antagonistically modulate the transcription and translation of IL-23. The signaling of STAT3-BATF2-c-JUN/ATF2-IL-23 ... heterodimerization of c-JUN and ATF2. ...

    Abstract Tea polyphenol of epigallocatechin-3-gallate (EGCG) has been verified to possess multiple biological activities. Interleukin-23 (IL-23) is a heterodimeric cytokine consisting of two subunits of IL-23p19 and IL-12p40, with the functionality in regulating the production of cytokines under physiological or pathological conditions. By serendipity, the raised expression of IL-23 was observed after treating cells with EGCG, whereas the detailed mechanism remains poorly understood. This study was proposed to investigate the signaling related to EGCG-induced IL-23. The raised expression of IL-23 was confirmed primarily by intraperitoneally injecting with different concentrations of EGCG (0, 20, 50, 80 mg/kg) into BALB/c mice, and the raised expression was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Results from enzyme-linked immunosorbent assay (ELISA) revealed the increase of IL-23 in serum from 116.09 to 153.90 pg/mL after treating with EGCG. The same results were also observed in RAW264.7 and peritoneal macrophages after treating with EGCG (0, 1, 5, 10, 25 μM) with the increased tendency of IL-23 in cultural medium (7.98 to 25.38 pg/mL for RAW264.7; 3.64 to 260.93 pg/mL for peritoneal macrophages). After preliminary exploration of the signaling related to the increased IL-23, the classical signaling pathways and key transcription factors, such as nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK) signaling pathways, and interferon regulatory factor 5 (IRF5), were demonstrated with no relevant contribution. A further study revealed the involvement of the key transcription factor of BATF2, which could antagonistically modulate the transcription and translation of IL-23. The signaling of STAT3-BATF2-c-JUN/ATF2-IL-23 has been further verified in RAW264.7 macrophages using the STAT3 inhibitor of AG490 and the activator of Colivelin TFA. The results indicated that EGCG inhibits the phosphorylation of STAT3 to facilitate the decreased level of BATF2, which contributed to the increased level of IL-23 by the enhancing heterodimerization of c-JUN and ATF2.
    MeSH term(s) Activating Transcription Factor 2 ; Animals ; Basic-Leucine Zipper Transcription Factors ; Catechin/analogs & derivatives ; Interferon Regulatory Factors ; Interleukin-23/genetics ; Mice ; Mice, Inbred BALB C ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-jun ; STAT3 Transcription Factor
    Chemical Substances Activating Transcription Factor 2 ; Atf2 protein, mouse ; BATF2 protein, mouse ; Basic-Leucine Zipper Transcription Factors ; Interferon Regulatory Factors ; Interleukin-23 ; Irf5 protein, mouse ; NF-kappa B ; Proto-Oncogene Proteins c-jun ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Catechin (8R1V1STN48) ; epigallocatechin gallate (BQM438CTEL)
    Language English
    Publishing date 2021-07-06
    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.1c02433
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1172: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  8. Article ; Online: Alantolactone exhibits antiproliferative and apoptosis-promoting properties in colon cancer model via activation of the MAPK-JNK/c-Jun signaling pathway.

    Ren, Yijing / Lv, Cheng / Zhang, Jing / Zhang, Beibei / Yue, Bei / Luo, Xiaoping / Yu, Zhilun / Wang, Hao / Ren, Junyu / Wang, Zhengtao / Dou, Wei

    Molecular and cellular biochemistry

    2021  Volume 476, Issue 12, Page(s) 4387–4403

    Abstract: ... the MAPK-JNK/c-Jun signaling pathway were measured by Western blot and RT-qPCR both in cells and tumor ... apoptosis effect by activating MAPK-JNK/c-Jun signaling pathway. In conclusion, ATL exhibits anti ... proliferation and apoptosis-promoting potential in colon cancer via the activation of MAPK-JNK/c-Jun ...

    Abstract Colorectal cancer (CRC) is one of the most common human malignancies in the digestive tract with high mortality. Alantolactone (ATL), as a plant-derived sesquiterpene lactone, has shown a variety of pharmacological activities, such as antibacterial, anti-inflammatory, anti-virus and so on. However, the exact molecular mechanism of ATL in colorectal cancer remains largely unknown. Here, we performed a study to explore the effect and mechanism of ATL on colorectal cancer. The CCK-8 assay, colony formation assay, Wound-healing and Transwell assays were performed to evaluate the cytotoxic effect, antiproliferative effect, anti-migratory and anti-invasive properties of ATL respectively. The xenograft tumor model was established in Balb/c mice to evaluate the anti-tumor effect. The expression levels of proteins involved the MAPK-JNK/c-Jun signaling pathway were measured by Western blot and RT-qPCR both in cells and tumor tissues. The results showed that ATL could inhibit the cells activities of various colon cancer cell lines. Moreover, ATL could induce HCT-116 cells nuclear pyknosis, mitochondrial membrane potential loss, G0/G1 phase arrest, as well as enhance the proportion of apoptosis cells and inhibit colony formation. The migration distance and invasion rate of cells were significantly reduced after treated with ATL. Additionally, in the xenograft model, ATL (50 mg/kg) significantly decreased the tumor tumor volume and weight (p < 0.001). For the anti-colon cancer mechanism, the ATL showed the anti-proliferative and pro-apoptosis effect by activating MAPK-JNK/c-Jun signaling pathway. In conclusion, ATL exhibits anti-proliferation and apoptosis-promoting potential in colon cancer via the activation of MAPK-JNK/c-Jun signaling pathway.
    MeSH term(s) Animals ; Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Lactones/pharmacology ; MAP Kinase Signaling System ; Mice ; Mice, Inbred BALB C ; Sesquiterpenes, Eudesmane/pharmacology ; Signal Transduction ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents, Phytogenic ; Lactones ; Sesquiterpenes, Eudesmane ; alantolactone (M7GSN5Q1M6)
    Language English
    Publishing date 2021-08-30
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 184833-1
    ISSN 1573-4919 ; 0300-8177
    ISSN (online) 1573-4919
    ISSN 0300-8177
    DOI 10.1007/s11010-021-04247-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 892: Show issues Location:
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  9. Article ; Online: Special role of JUN in papillary thyroid carcinoma based on bioinformatics analysis.

    Chen, Wenzheng / Liu, Qingfeng / Lv, Yunxia / Xu, Debin / Chen, Wanzhi / Yu, Jichun

    World journal of surgical oncology

    2017  Volume 15, Issue 1, Page(s) 119

    Abstract: ... hepatocyte nuclear factor 4, alpha (HNF4A) and DEG JUN had higher connection degrees. Clustering analysis indicated that two ... function modules, in which JUN was playing a central role, were highly relevant to PTC genesis and ... progression.: Conclusions: JUN may be used as a specific diagnostic biomarker/therapeutic molecular target ...

    Abstract Background: Papillary thyroid carcinoma (PTC) is the most common malignancy in thyroid tissue, and the number of patients with PTC has been increasing in recent years. Discovering the mechanism of PTC genesis and progression and finding new potential diagnostic biomarkers/therapeutic target genes of PTC are of great significance.
    Methods: In this work, the datasets GSE3467 and GSE3678 were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified with the limma package in R. GO function and KEGG pathway enrichment were conducted with DAVID tool. The interaction network of the DEGs and other genes was performed with Cytoscape plugin BisoGenet, while clustering analysis was performed with Cytoscape plugin ClusterOne.
    Results: A total of 1800 overlapped DEGs were detected in two datasets. Enrichment analysis of the DEGs found that the top three enriched GO terms in three ontologies and four significantly enriched KEGG pathways were mainly concerned with intercellular junction and extracellular matrix components. Interaction network analysis found that transcription factor hepatocyte nuclear factor 4, alpha (HNF4A) and DEG JUN had higher connection degrees. Clustering analysis indicated that two function modules, in which JUN was playing a central role, were highly relevant to PTC genesis and progression.
    Conclusions: JUN may be used as a specific diagnostic biomarker/therapeutic molecular target of PTC. However, further experiments are still needed to confirm our results.
    Language English
    Publishing date 2017-07-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2118383-1
    ISSN 1477-7819 ; 1477-7819
    ISSN (online) 1477-7819
    ISSN 1477-7819
    DOI 10.1186/s12957-017-1190-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: TRPM2-AS inhibits the growth, migration, and invasion of gliomas through JNK, c-Jun, and RGS4.

    Bao, Mei-Hua / Lv, Qiao-Li / Szeto, Vivian / Wong, Raymond / Zhu, Su-Zhen / Zhang, Ying-Ying / Feng, Zhong-Ping / Sun, Hong-Shuo

    Journal of cellular physiology

    2019  Volume 235, Issue 5, Page(s) 4594–4604

    Abstract: ... western-blot analysis indicated the increase of RGS4 protein expression and decrease of p-JNK/JNK and p-c-Jun/c-Jun ... suppressed the expression of RGS4 and promoted the ratios of p-JNK/JNK and p-c-Jun/c-Jun. The present work ... partly, be related to JNK, c-Jun, and RGS4. Our work provided new insights into the underlying mechanisms ...

    Abstract Gliomas are a group of brain cancers with high mortality and morbidity. Understanding the molecular mechanisms is important for the prevention or treatment of gliomas. The present study was to investigate the effects and mechanisms of long noncoding RNA TRPM2-AS in gliomas proliferation, migration, and invasion. We first compared the levels of TRPM2-AS in 111 patients with glioma to that of the normal control group by a quantitative polymerase chain reaction. The results indicated a significant increase of TRPM2-AS in patients with glioma (2.43 folds of control, p = .0135). MTT methods, wound healing assays, transwell analysis, and clone formation analysis indicated the overexpression of TRPM2-AS promoted the proliferation, migration, and invasion of U251 and U87 cells, while downregulation of TRPM2-AS inhibited the cell proliferation, migration, and invasion significantly (p < .05). To further uncover the mechanisms, bioinformatics analysis was conducted on the expression profiles, GSE40687 and GSE4290, from the Gene Expression Omnibus database. One hundred fifty-six genes were differentially expressed in both datasets (FC > 2.0; p = .05). Among these differentially expressed genes, the level of RGS4 messenger RNA was drastically regulated by TRPM2-AS. Further western-blot analysis indicated the increase of RGS4 protein expression and decrease of p-JNK/JNK and p-c-Jun/c-Jun ratio after TRPM2-AS overexpression. On the other hand, inhibition of TRPM2-AS by small interfering RNA suppressed the expression of RGS4 and promoted the ratios of p-JNK/JNK and p-c-Jun/c-Jun. The present work indicated the mechanisms of the participation of TRPM2-AS in the progression of gliomas might, at least partly, be related to JNK, c-Jun, and RGS4. Our work provided new insights into the underlying mechanisms of glioma cellular functions.
    MeSH term(s) Adult ; Brain Neoplasms/enzymology ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Case-Control Studies ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Databases, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Glioma/enzymology ; Glioma/genetics ; Glioma/pathology ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Middle Aged ; Neoplasm Invasiveness ; Phosphorylation ; Proto-Oncogene Proteins c-jun/metabolism ; RGS Proteins/genetics ; RGS Proteins/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Signal Transduction
    Chemical Substances JUN protein, human ; Proto-Oncogene Proteins c-jun ; RGS Proteins ; RNA, Long Noncoding ; RGS4 protein (175335-35-0) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2019-10-21
    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.29336
    Database MEDical Literature Analysis and Retrieval System OnLINE

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