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RISS 인기검색어
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- 저자 : Yingnan Yang (검색결과 4 건)
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Ping Yang,Yingnan Qiao,Huaidong Liao,Yizheng Huang,Mei Meng,Yu Chen,Quansheng Zhou 한국유방암학회 2023 Journal of breast cancer Vol.26 No.2
Purpose: Invasive breast carcinomas (BRCAs) are highly lethal. The molecular mechanisms underlying progression of invasive BRCAs are unclear, and effective therapies are highly desired. The cancer-testis antigen CT45A1 promotes overexpression of pro-metastatic sulfatase-2 (SULF2) and breast cancer metastasis to the lungs, but its mechanisms are largely unknown. In this study, we aimed to elucidate the mechanism of CT45A1-induced SULF2 overexpression and provide evidence for targeting CT45A1 and SULF2 for breast cancer therapy. Methods: The effect of CT45A1 on SULF2 expression was assessed using reverse transcription polymerase chain reaction and western blot. The mechanism of CT45A1-induced SULF2 gene transcription was studied using protein-DNA binding assay and a luciferase activity reporter system. The interaction between CT45A1 and SP1 proteins was assessed using immunoprecipitation and western blot. Additionally, the suppression of breast cancer cell motility by SP1 and SULF2 inhibitors was measured using cell migration and invasion assays. Results: CT45A1 and SULF2 are aberrantly overexpressed in patients with BRCA; importantly, overexpression of CT45A1 is closely associated with poor prognosis. Mechanistically, gene promoter demethylation results in overexpression of both CT45A1 and SULF2. CT45A1 binds directly to the core sequence GCCCCC in the promoter region of SULF2 gene and activates the promoter. Additionally, CT45A1 interacts with the oncogenic master transcription factor SP1 to drive SULF2 gene transcription. Interestingly, SP1 and SULF2 inhibitors suppress breast cancer cell migration, invasion, and tumorigenicity. Conclusion: Overexpression of CT45A1 is associated with poor prognosis in patients with BRCA. CT45A1 promotes SULF2 overexpression by activating the promoter and interacting with SP1. Additionally, SP1 and SULF2 inhibitors suppress breast cancer cell migration, invasion, and tumorigenesis. Our findings provide new insight into the mechanisms of breast cancer metastasis and highlight CT45A1 and SULF2 as sensible targets for developing novel therapeutics against metastatic breast cancer.
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Nanotherapeutics with immunoregulatory functions for the treatment of bacterial infection
Dongliang Yang,Meng Ding,Yanni Song,Yanling Hu,Weijun Xiu,Lihui Yuwen,Yannan Xie,Yingnan Song,Jinjun Shao,Xuejiao Song,Heng Dong 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
The advent of drug-resistant pathogens results in the occurrence of stubborn bacterial infections that cannot betreated with traditional antibiotics. Antibacterial immunotherapy by reviving or activating the body’s immune systemto eliminate pathogenic bacteria has confrmed promising therapeutic strategies in controlling bacterial infections. Subsequent studies found that antimicrobial immunotherapy has its own benefts and limitations, such as avoidingrecurrence of infection and autoimmunity-induced side efects. Current studies indicate that the various antibacterialtherapeutic strategies inducing immune regulation can achieve superior therapeutic efcacy compared with mono therapy alone. Therefore, summarizing the recent advances in nanomedicine with immunomodulatory functionsfor combating bacterial infections is necessary. Herein, we briefy introduce the crisis caused by drug-resistantbacteria and the opportunity for antibacterial immunotherapy. Then, immune-involved multimodal antibacterialtherapy for the treatment of infectious diseases was systematically summarized. Finally, the prospects and challengesof immune-involved combinational therapy are discussed.
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Li Qiqi,Zhang Yingnan,Song Ya,Yang Huawei,Yang Lixia,Bai Liangjiu,Wei Donglei,Wang Wenxiang,Liang Ying,Chen Hou 한국탄소학회 2023 Carbon Letters Vol.33 No.2
Biomass carbon materials with high rate capacity have great potential to boost supercapacitors with cost effective, fast charging–discharging performance and high safety requirements, yet currently suffers from a lack of targeted preparation methods. Here we propose a facile FeCl3 assisted hydrothermal carbonization strategy to prepare ultra-high rate biomass carbon from apple residues (ARs). In the preparation process, ARs were first hydrothermally carbonized into a porous precursor which embedded by Fe species, and then synchronously graphitized and activated to form biocarbon with a large special surface area (2159.3 m2 g−1) and high degree of graphitization. The material exhibited a considerable specific capacitance of 297.5 F g−1 at 0.5 A g−1 and outstanding capacitance retention of 85.7% at 10 A g−1 in 6 M KOH, and moreover, achieved an energy density of 16.2 Wh kg−1 with the power density of 350.3 W kg−1. After 8000 cycles, an initial capacitance of 95.2% was maintained. Our findings provide a new idea for boosting the rate capacity of carbon-based electrode materials.
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Huajie Cai,Yihu Zheng,Zhengde Wen,Yingnan Yang,Shouzhang Yang,Qiyu Zhang 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.4
Long non-coding RNAs (LncRNAs) havebeen implicated in the pathogenesis of various human diseases. In this study, we probed into the role and potentialmechanisms of the antisense of IGF2R non-protein codingRNA (LncRNA AIRN) in the progression of hepatocellularcarcinoma (HCC). Using a quantitative real-timepolymerase chain reaction, we corroborated that LncRNAAIRN expression was raised in the HCC tissues and cells. The bioinformatic analysis revealed that a potential interactionbetween LncRNA AIRN and STAT1, which wasverifi ed by the RNA pull-down and RNA immunoprecipitation. In the cycloheximide-chase assay, the knockdown ofLncRNA AIRN enhanced the stability of STAT1 protein. Inthe immunoprecipitation assay, the knockdown of LncRNAAIRN restrained the cullin 4A (CUL4A)-mediated ubiquitinationof STAT1 protein. The cell transfection, MTT andfl ow cytometry assays expounded that the LncRNA AIRN/STAT1 axis was bound up with the regulation of the proliferationand apoptosis of HCC cells. The in vivo experimentscorroborated that the knockdown of LncRNA AIRNrestrained the tumor growth of HCC. Our data expoundedthat the knockdown of LncRNA AIRN restrained HCC cellproliferation and boosted cell apoptosis by restraining theCUL4A-mediated ubiquitination of STAT1 protein.
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