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      • KCI등재

        Sp1-Induced SETDB1 Overexpression Transcriptionally Inhibits HPGD in a β-Catenin-Dependent Manner and Promotes the Proliferation and Metastasis of Gastric Cancer

        Fan Yaguan,Yang Libo,Ren Yi,Wu Yunhua,Li Linhai,Li Lihua 대한위암학회 2022 Journal of gastric cancer Vol.22 No.4

        Purpose Gastric cancer (GC) has high morbidity and mortality, the cure rate of surgical treatment and drug chemotherapy is not ideal. Therefore, development of new treatment strategies is necessary. We aimed to identify the mechanism underlying Sp1 regulation of GC progression. Methods and Methods The levels of Sp1, β-catenin, SET domain bifurcated 1 (SETDB1), and 15-hydroxyprostaglandin dehydrogenase (HPGD) were detected by quantitative reverse transcription polymerase chain reaction and western blot analysis. The targets of SETDB1 were predicted by AnimalTFDB, and dual-luciferase reporter assay was used for confirming the combination of Sp1, β-catenin, and SETDB1. HGC27 or AGS cells (1×106 cells/mouse) were injected into mice via the caudal vein for GC model establishment. The level of Ki67 was detected using immunohistochemistry, and hematoxylin and eosin staining was performed for evaluating tumor metastasis in mice with GC. Results HPGD was inhibited, while the protein levels of Sp1, β-catenin, and SETDB1 were up-regulated in GC tissues and cell lines. HPGD overexpression or SETDB1 silencing inhibited the proliferation, invasion, and migration of GC cells, and Sp1 regulated the proliferation, invasion, and migration of GC cells in a β-catenin-dependent manner. Furthermore, HPGD served as a target of SETDB1, and it was negatively regulated by SETDB1; additionally, Sp1 and β-catenin bound to the SETDB1 promoter and negatively regulated HPGD expression. We proved that Sp1 regulated GC progression via the SETDB1/HPGD axis. Conclusions Our findings revealed that Sp1 transcriptionally inhibited HPGD via SETDB1 in a β-catenin-dependent manner and promoted the proliferation and metastasis of GC cells. Purpose Gastric cancer (GC) has high morbidity and mortality, the cure rate of surgical treatment and drug chemotherapy is not ideal. Therefore, development of new treatment strategies is necessary. We aimed to identify the mechanism underlying Sp1 regulation of GC progression. Methods and Methods The levels of Sp1, β-catenin, SET domain bifurcated 1 (SETDB1), and 15-hydroxyprostaglandin dehydrogenase (HPGD) were detected by quantitative reverse transcription polymerase chain reaction and western blot analysis. The targets of SETDB1 were predicted by AnimalTFDB, and dual-luciferase reporter assay was used for confirming the combination of Sp1, β-catenin, and SETDB1. HGC27 or AGS cells (1×106 cells/mouse) were injected into mice via the caudal vein for GC model establishment. The level of Ki67 was detected using immunohistochemistry, and hematoxylin and eosin staining was performed for evaluating tumor metastasis in mice with GC. Results HPGD was inhibited, while the protein levels of Sp1, β-catenin, and SETDB1 were up-regulated in GC tissues and cell lines. HPGD overexpression or SETDB1 silencing inhibited the proliferation, invasion, and migration of GC cells, and Sp1 regulated the proliferation, invasion, and migration of GC cells in a β-catenin-dependent manner. Furthermore, HPGD served as a target of SETDB1, and it was negatively regulated by SETDB1; additionally, Sp1 and β-catenin bound to the SETDB1 promoter and negatively regulated HPGD expression. We proved that Sp1 regulated GC progression via the SETDB1/HPGD axis. Conclusions Our findings revealed that Sp1 transcriptionally inhibited HPGD via SETDB1 in a β-catenin-dependent manner and promoted the proliferation and metastasis of GC cells.

      • SCOPUSKCI등재

        Sp1-Induced SETDB1 Overexpression Transcriptionally Inhibits HPGD in a β-Catenin-Dependent Manner and Promotes the Proliferation and Metastasis of Gastric Cancer

        Fan, Yaguan,Yang, Libo,Ren, Yi,Wu, Yunhua,Li, Linhai,Li, Lihua The Korean Gastric Cancer Association 2022 Journal of gastric cancer Vol.22 No.-

        Purpose: Gastric cancer (GC) has high morbidity and mortality, the cure rate of surgical treatment and drug chemotherapy is not ideal. Therefore, development of new treatment strategies is necessary. We aimed to identify the mechanism underlying Sp1 regulation of GC progression. Methods and Methods: The levels of Sp1, β-catenin, SET domain bifurcated 1 (SETDB1), and 15-hydroxyprostaglandin dehydrogenase (HPGD) were detected by quantitative reverse transcription polymerase chain reaction and western blot analysis. The targets of SETDB1 were predicted by AnimalTFDB, and dual-luciferase reporter assay was used for confirming the combination of Sp1, β-catenin, and SETDB1. HGC27 or AGS cells (1×10<sup>6</sup> cells/mouse) were injected into mice via the caudal vein for GC model establishment. The level of Ki67 was detected using immunohistochemistry, and hematoxylin and eosin staining was performed for evaluating tumor metastasis in mice with GC. Results: HPGD was inhibited, while the protein levels of Sp1, β-catenin, and SETDB1 were up-regulated in GC tissues and cell lines. HPGD overexpression or SETDB1 silencing inhibited the proliferation, invasion, and migration of GC cells, and Sp1 regulated the proliferation, invasion, and migration of GC cells in a β-catenin-dependent manner. Furthermore, HPGD served as a target of SETDB1, and it was negatively regulated by SETDB1; additionally, Sp1 and β-catenin bound to the SETDB1 promoter and negatively regulated HPGD expression. We proved that Sp1 regulated GC progression via the SETDB1/HPGD axis. Conclusions: Our findings revealed that Sp1 transcriptionally inhibited HPGD via SETDB1 in a β-catenin-dependent manner and promoted the proliferation and metastasis of GC cells.

      • KCI등재
      • Design and Implementation of Campus Information System with Android and Web Dual-mode Based on MVC Pattern

        Feng Jian,Ren Jian,Fan Ren-Yi,Lei Jing 보안공학연구지원센터 2015 International Journal of u- and e- Service, Scienc Vol.8 No.7

        Mobile application for campus is an integral part of the construction of wisdom campus. CampusService - a campus information service system is designed, and is comprised of three parts, Android client, Web client and server, which are all designed according to MVC pattern. C/S architecture is adopted between the Android client and the server, B/S architecture is adopted between the Web client and the server, and JSON is used as a unified data interface for accomplishing the interactions. The architectures of three parts are described, and key technologies are represented, including database access optimization, Android display, transaction management and authentication, among which database access optimization technology has two respects: using C3P0 to maintain connection pool and prefetching data based on their popularity. According to testing, the system implements functions of user management, intramural announcements, interaction with friends, activity participation, and campus maps, and it has good performance. The system provides an efficient platform for real-time communication among teachers, students and school authority.

      • KCI등재

        A R2R3-type MYB transcription factor gene from soybean, GmMYB12, is involved in flavonoids accumulation and abiotic stress tolerance in transgenic Arabidopsis

        Feibing Wang,Xuqin Ren,Fan Zhang,Mingyang Qi,Huiyun Zhao,Xinhong Chen,Yuxiu Ye,Jiayin Yang,Shuguang Li,Yi Zhang,Yuan Niu,Qing Zhou 한국식물생명공학회 2019 Plant biotechnology reports Vol.13 No.3

        The R2R3-type MYB transcription factors have been shown to increase flavonoids accumulation by regulating the expression of key enzyme genes related to flavonoid biosynthesis pathway. However, the roles and underlying mechanisms of the soybean GmMYB12 gene in regulation of flavonoids accumulation and tolerance to abiotic stresses are rarely known. In the present study, the GmMYB12 gene was isolated and its function was characterized. Sequence and yeast one-hybrid analyses showed that GmMYB12 contained two MYB domains and belonged to R2R3-MYB protein with transactivation activity. Subcellular localization analysis in onion epidermal cells indicated that GmMYB12 was localized to the nucleus. Overexpression of GmMYB12 increased the production of downstream flavonoids and the expression of related genes in the flavonoid biosynthesis pathway. It also improved resistance to salt and drought stresses during seed germination, root development, and growing stage. Further component and enzymatic analyses showed significant increases of proline content, pyrroline-5-carboxylate synthase (P5CS), superoxide dismutase (SOD), and peroxidase (POD) activities, as well as significant reduction of H2O2 and malonaldehyde (MDA) content under salt and drought stresses in transgenic plants. Meanwhile, the expression level of AtP5CS, AtSOD and AtPOD genes was up-regulated against salt and drought stresses. Together, our finding indicated that changing the expression level of GmMYB12 in plants alters the accumulation of flavonoids and regulates plantlet tolerance to abiotic stress by regulating osmotic balance, protecting membrane integrity and maintaining ROS homeostasis. The GmMYB12 gene has the potential to be used to increase the content of valuable flavonoids and improve the tolerance to abiotic stresses in plants

      • Dynamic deflection monitoring method for long-span cable-stayed bridge based on bi-directional long short-term memory neural network

        Wen-Yu He,Yi-Fan Li,Wei-Xin Ren,Gang Liu,Hai-Peng Sun 국제구조공학회 2023 Smart Structures and Systems, An International Jou Vol.32 No.5

        Dynamic deflection is important for evaluating the performance of a long-span cable-stayed bridge, and its continuous measurement is still cumbersome. This study proposes a dynamic deflection monitoring method for cable-stayed bridge based on Bi-directional Long Short-term Memory (BiLSTM) neural network taking advantages of the characteristics of spatial variation of cable acceleration response (CAR) and main girder deflection response (MGDR). Firstly, the relationship between the spatial and temporal variation of the CAR and the MGDR is described based on the geometric deformation of the bridge. Then a data-driven relational model based on BiLSTM neural network is established using CAR and MGDR data, and it is further used to monitor the MGDR via measuring the CAR. Finally, numerical simulations and field test are conducted to verify the proposed method. The root mean squared error (RMSE) of the numerical simulations are less than 4 while the RMSE of the field test is 1.5782, which indicate that it provides a cost-effective and convenient method for real-time deflection monitoring of cable-stayed bridges.

      • Decreased Expression of FADS1 Predicts a Poor Prognosis in Patients with Esophageal Squamous Cell Carcinoma

        Du, Yong,Yan, Shu-Mei,Gu, Wan-Yi,He, Fan,Huang, Li-Yun,Li, Mei,Yuan, Yan,Chen, Ren-Hui,Zhong, Qian,Li, Man-Zhi,Li, Yong,Zeng, Mu-Sheng Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.12

        FADS1 (fatty acid desaturase 1) plays a crucial role in fatty acid metabolism, and it was recently reported to be involved in tumorigenesis. However, the role of FADS1 expression in esophageal squamous cell carcinoma (ESCC) remains unknown. In the current study, we investigated the expression and clinical pathologic and prognostic significance of FADS1 in ESCC. Immunohistochemical analyses revealed that 58.2% (146/251) of the ESCC tissues had low levels of FADS1 expression, whereas 41.8% (105/251) exhibited high levels of FADS1 expression. In positive cases, FADS1 expression was detected in the cytoplasm of cells. Correlation analyses demonstrated that FADS1 expression was significantly correlated with tumor location (p=0.025) but not with age, gender, histological grade, tumor status, nodal status or TNM staging. Furthermore, patients with tumors expressing high levels of FADS1had a longer disease-free survival time (p<0.001) and overall survival time (p <0.001). Univariate and multivariate analyses revealed that, along with nodal status, FADS1 expression was an independent and significant predictive factor (p<0.001). In conclusion, our study suggested that FADS1 might be a valuable biomarker and potential therapeutic target for ESCC.

      • KCI등재

        De novo assembly and transcriptome analysis of differentially expressed genes relevant to variegation in hawthorn flowers

        Wei Ji,Wei Zhao,Rong‑Chen Liu,Xiao‑Bo Jiao,Kai Han,Zhong‑Yi Yang,Mei‑Ying Gao,Rui Ren,Xiu‑Juan Fan,Ming‑Xia Yang 한국식물생명공학회 2019 Plant biotechnology reports Vol.13 No.6

        Flower color variegation has been observed in many plant species. However, pink flowers on the white-blooming hawthorn trees found by our group earlier have never been reported. To better understand the differentially expressed genes (DEGs) in variegated hawthorn flowers, white and pink flowers at different developmental stages (S1 and S2) underwent transcriptome sequencing separately. Approximately 34.28 Gb of high-quality data were obtained and assembled into 100,013 unigenes with an average length of 706.93 bp. These unigenes were further subjected to functional annotation and biochemical pathway analysis, and DEGs of two types of hawthorn flowers at different developmental stages were studied. Based on the enrichment analysis of DEGs, eight anthocyanin-modified enzyme genes or other enzyme genes that indirectly affect anthocyanin synthesis (5AT, 3GGT , and AI, β-Glu, two Aux/IAAs, two PODs), eight structural genes (UFGT, DFR, CHI, two F3Hs, and three PALs), and three transcription factors (one MYB and two bHLHs) were also identified. We randomly selected 15 genes, and the trends in the expression levels of these genes in the organs of white and pink flowers at different developmental stages were verified by quantitative real-time PCR. Mass sequence data obtained by RNA-seq of variegated hawthorn flowers provided basic sequence information and a unique opportunity to uncover the genetic mechanisms under-lying flower color variegation.

      • KCI등재

        Prolyl endopeptidase remodels macrophage function as a novel transcriptional coregulator and inhibits fibrosis

        Lin Shuang-Zhe,Wu Wei-Jie,Cheng Yu-Qing,Zhang Jian-Bin,Jiang Dai-Xi,Ren Tian-Yi,Ding Wen-Jin,Liu Mingxi,Chen Yuan-Wen,Fan Jian-Gao 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

        Macrophages are immune cells crucial for host defense and homeostasis maintenance, and their dysregulation is involved in multiple pathological conditions, such as liver fibrosis. The transcriptional regulation in macrophage is indispensable for fine-tuning of macrophage functions, but the details have not been fully elucidated. Prolyl endopeptidase (PREP) is a dipeptidyl peptidase with both proteolytic and non-proteolytic functions. In this study, we found that Prep knockout significantly contributed to transcriptomic alterations in quiescent and M1/M2-polarized bone marrow-derived macrophages (BMDMs), as well as aggravated fibrosis in an experimental nonalcoholic steatohepatitis (NASH) model. Mechanistically, PREP predominantly localized to the macrophage nuclei and functioned as a transcriptional coregulator. Using CUT&Tag and co-immunoprecipitation, we found that PREP was mainly distributed in active cis-regulatory genomic regions and physically interacted with the transcription factor PU.1. Among PREP-regulated downstream genes, genes encoding profibrotic cathepsin B and D were overexpressed in BMDMs and fibrotic liver tissue. Our results indicate that PREP in macrophages functions as a transcriptional coregulator that finely tunes macrophage functions, and plays a protective role against liver fibrosis pathogenesis.

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