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- 저자 : Yuting Tan (검색결과 3 건)
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Linyue Pan,Yuting Tan,Bin Wang,Wenjia Qiu,Yulei Yin,Haiyan Ge,Huili Zhu 대한암학회 2020 Cancer Research and Treatment Vol.52 No.3
Purpose Caspase recruitment domain containing protein 9 (CARD9) has been demonstrated to be a pro-tumor factor in various cancers. However, our previous study found a significant decrease of CARD9 in malignant pleural effusion compared with benign pleural effusion. So we investigated the role of CARD9 in non-small cell lung cancer (NSCLC) and its working mechanism. Materials and Methods Immunohistochemistry, western blot, and quantitative real-time polymerase chain reaction were used to detect the expression of CARD9 in specimens of NSCLC patients. The Cancer Genome Atlas (TCGA) database was also used to analyze the expression of CARD9 in NSCLC and its predicting value for prognosis. Immunofluorescence was used for CARD9 cellular location. Cell growth assay, clonal formation assay, wound healing assay, matrigel invasion assay, and flow cytometry were used to test cell proliferation, migration, invasion, apoptosis, and cycle progression of NSCLC cells with CARD9 knockdown or CARD9 overexpression. Co-immunoprecipitation was used to identify the interaction between CARD9 and B-cell lymphoma 10 (BCL10). SB203580 was used to inhibit p38 activation. Results CARD9 was decreased in NSCLC tissues compared with normal tissues; low CARD9 expression was associated with poor survival. CARD9 was expressed both in tumor cells and macrophages. Downregulation of CARD9 in NSCLC cells enhanced the abilities of proliferation, invasion, and migration via activated mitogen-activated protein kinases (MAPK)/p38 signaling, while overexpression of CARD9 presented antitumor effects. BCL10 was identified to interact with CARD9. Conclusion We demonstrate that CARD9 is an independent prognostic factor in NSCLC patients and inhibits proliferation, migration, and invasion by suppressing MAPK/p38 pathway in NSCLC cells.
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( Kai Yang ),( Yulong Tang ),( Yanyun Ma ),( Qingmei Liu ),( Yan Huang ),( Yuting Zhang ),( Xiangguang Shi ),( Li Zhang ),( Yue Zhang ),( Ji’an Wang ),( Yifei Zhu ),( Wei Liu ),( Yimei Tan ),( Jinran 대한피부과학회 2021 Annals of Dermatology Vol.33 No.6
Background: Androgenetic alopecia (AGA) leads to thinning of scalp hair and affects 60%~70% of the adult population worldwide. Developing more effective treatments and studying its mechanism are of great significance. Previous clinical studies have revealed that hair growth is stimulated by 650-nm red light. Objective: This study aimed to explore the effect and mechanism of 650-nm red light on the treatment of AGA by using ex vivo hair follicle culture. Methods: Human hair follicles were obtained from hair transplant patients with AGA. Hair follicles were cultured in Williams E medium and treated with or without 650-nm red light. Real-time RT-PCR and immunofluorescence staining were used to detect the expression level of genes and proteins in hair follicles, respectively. RNA-sequencing analysis was carried out to reveal the distinct gene signatures upon 650 nm treatment. Results: Low-level 650 nm red light promoted the proliferation of human hair follicles in the experimental cultured-tissue model. Consistently, 650 nm red light significantly delayed the transition of hair cycle from anagen to catagen in vitro. RNA-seq analysis and gene clustering for the differentially expressed genes suggests that leukocyte transendothelial migration, metabolism, adherens junction and other biological process maybe involved in stimulation of hair follicles by 650-nm red light treatment. Conclusion: The effect of 650-nm red light on ex vivo hair follicles and the transcriptome set which implicates the role of red light in promoting hair growth and reversing of miniaturization process of AGA were identified.
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Honglin Xu,Haifeng Miao,Guanghong Chen,Guoyong Zhang,Yue Hua,Yuting Wu,Tong Xu,Changlei Hu,Mingjie Pang,Leyi Tan,Xin Han,Bin Liu,Yingchun Zhou 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiacremodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovasculardiseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effectpost-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-b1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin andMasson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effectsof Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 wasexplored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice andTGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiacfunction. Rg3-TGFBR1 had the 1.78 10 7 M equilibrium dissociation constant based on SPRi analysis,and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulatedthe TGF-b1-mediated CFs growth together with collagen production in vitro through TGFBR1signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferationalong with collagen deposition by inactivation of TGFBR1 pathway.
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