نتائج البحث - "Cai, Xueting"

1

دورية أكاديمية

KRAS-mutant non-small cell lung cancer (NSCLC) therapy based on tepotinib and omeprazole combination ...

مصطلحات موضوعية: Biophysics, Biochemistry, Cell Biology, Molecular Biology, Pharmacology, Chemical Sciences not elsewhere classified, Cancer, Hematology

الوصف: Background KRAS-mutant non-small cell lung cancer (NSCLC) shows a relatively low response rate to chemotherapy, immunotherapy and KRAS-G12C selective inhibitors, leading to short median progression-free survival, and overall survival. The MET receptor tyrosine kinase (c-MET), the cognate receptor of hepatocyte growth factor (HGF), was reported to be overexpressed in KRAS-mutant lung cancer cells leading to tumor-growth in anchorage-independent conditions. Methods Cell viability assay and synergy analysis were carried out in native, sotorasib and trametinib-resistant KRAS-mutant NSCLC cell lines. Colony formation assays and Western blot analysis were also performed. RNA isolation from tumors of KRAS-mutant NSCLC patients was performed and KRAS and MET mRNA expression was determined by real-time RT-qPCR. In vivo studies were conducted in NSCLC (NCI-H358) cell-derived tumor xenograft model. Results Our research has shown promising activity of omeprazole, a V-ATPase-driven proton pump inhibitor with ...

الإتاحة: https://doi.org/10.6084/m9.figshare.c.7283195Test
https://springernature.figshare.com/collections/KRAS-mutant_non-small_cell_lung_cancer_NSCLC_therapy_based_on_tepotinib_and_omeprazole_combination/7283195Test

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2

دورية أكاديمية

Study on morphology optimization of open-pit mine slope based on section and spatial morphology effect

المؤلفون: Jia, Lan, Wang, Jiaqi, Cai, Xueting, Fang, Linhao, Ma, Yonghai, Wang, Zhixin

المصدر: Scientific Reports ; volume 14, issue 1 ; ISSN 2045-2322

مصطلحات موضوعية: Multidisciplinary

الوصف: Reasonable design of the slopes of mining field is an important prerequisite for optimizing open-pit mine boundary, ensuring safe production and improving economic benefits of open-pit mines. This study took the open-pit coal mine coal mine in Block I of Thar coal field in Pakistan as the research background, based on the section morphology effect of slope stability and the occurrence characteristics of coal seam and weak layer, the section morphology of slope was optimized step by step from two-dimensional angle by using the rigid body limit equilibrium method. The three-dimensional numerical simulation method is used to analyze the three-dimensional spatial effect of slope stability and reveal the influence of the spatial geometry of the slope stability. The spatial morphology of the slope was optimized and the evolutionary mechanism of slope instability was revealed. By comparing the optimized slope morphology with the preliminary design and the slope morphology of the straight slope with equal flat plate, the economic benefits were further analyzed. The results showed that under the premise of meeting the safety reserve coefficient, compared with the preliminary design and the design of equal plate. The slope angle of the optimized section morphology was increased by 1° and 3° respectively, and the coal resource recovery was increased by 332 m 2 and 1790 m 2 respectively, and the economic benefits were $ 18,065,859 and $ 54,408,251 respectively. And the slope angle of the optimized spatial morphology was increased by 3° and 5° respectively, and the coal resource recovery was increased by 1188 m 2 and 2726 m 2 respectively, and the economic benefits were $ 72,082,808 and $ 108,417,368 respectively.

الإتاحة: https://doi.org/10.1038/s41598-024-53227-5Test
https://www.nature.com/articles/s41598-024-53227-5.pdfTest
https://www.nature.com/articles/s41598-024-53227-5Test

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3

دورية أكاديمية

Additional file 1 of KRAS-mutant non-small cell lung cancer (NSCLC) therapy based on tepotinib and omeprazole combination ...

مصطلحات موضوعية: Biophysics, Biochemistry, Cell Biology, Molecular Biology, Pharmacology, Chemical Sciences not elsewhere classified, Cancer, Hematology

الوصف: Supplementary Material 1 ...

الإتاحة: https://doi.org/10.6084/m9.figshare.2602746210.1158/2159-8290.cd-20-116510.1016/j.tranon.2021.10127610.1016/j.jtho.2022.03.01010.1158/1078-0432.ccr-20-402310.1158/2159-8290.cd-18-009910.1016/j.jtho.2021.10.01310.1158/0008-5472.can-22-173110.1158/1078-0432.ccr-21-307410.1056/nejmoa191723910.1056/nejmoa210369510.1056/nejmoa220461910.1200/jco.21.0275210.1038/s41586-021-04065-210.1158/2159-8290.cd-21-036510.1056/nejmoa210528110.1038/s43018-021-00289-310.1016/j.cell.2020.09.04410.1016/j.ccell.2019.12.00910.1158/2159-8290.cd-19-116710.1158/0008-5472.can-04-2650Test
https://springernature.figshare.com/articles/journal_contribution/Additional_file_1_of_KRAS-mutant_non-small_cell_lung_cancer_NSCLC_therapy_based_on_tepotinib_and_omeprazole_combination/26027462Test

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4

دورية أكاديمية

Ginseng-derived nanoparticles reprogram macrophages to regulate arginase-1 release for ameliorating T cell exhaustion in tumor microenvironment

المؤلفون: Lv, Yan, Li, Mengyuan, Weng, Ling, Huang, Haoying, Mao, Yujie, Yang, Danchen Aaron, Wei, Qingyun, Zhao, Mengmeng, Wei, Qin, Rui, Ke, Han, Xuan, Fan, Weiwei, Cai, Xueting, Cao, Peng, Cao, Meng

المساهمون: the National Natural Science Foundation of China, the Natural Science Foundation of Jiangsu Province, Technology Development Program of Traditional Chinese Medicine in Jiangsu Province, WINFAST Charity Foundation, Open Project of Chinese Materia Medica First-Class Discipline of Nanjing University of Chinese Medicine, Priority Academic Program Development of Jiangsu Higher Education Institutions

المصدر: Journal of Experimental & Clinical Cancer Research ; volume 42, issue 1 ; ISSN 1756-9966

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: Background Lines of evidence indicated that, immune checkpoints (ICs) inhibitors enhanced T cell immune response to exert anti-tumor effects. However, T cell exhaustion has been so far a major obstacle to antitumor immunotherapy in colorectal cancer patients. Our previous studies showed that ginseng-derived nanoparticles (GDNPs) inhibited the growth of various tumors by reprograming tumor-associated macrophages (TAMs) and downregulated the ICs expression on T cells in tumor microenvironment (TME), but the underlying effector mechanisms remained unclear. Methods The correlation between arginase-1 (ARG1) and T cells was computed based on the colorectal cancer patients in TCGA database. In vitro, we observed that GDNPs reprogrammed TAMs inhibited ARG1 release and ultimately ameliorated T cell exhaustion according to several techniques including WB, PCR, ELISA and flow cytometry. We also used an in vivo MC38 tumor-bearing model and administered GDNPs to assess their anti-tumor effects through multiple indices. The mechanism that GDNPs improved T cell exhaustion was further clarified using the bioinformatics tools and flow cytometry. Results GDNPs reprogramed TAMs via reducing ARG1 production. Moreover, normalized arginine metabolism ameliorated T cell exhaustion through mTOR-T-bet axis, resulting in reduced ICs expression and enhanced CD8 + T cells expansion. Conclusions By regulating the mTOR-T-bet axis, GDNPs reprogramed macrophages to regulate ARG1 release, which further ameliorated T cell exhaustion in TME. These findings provided new insights into comprehending the mechanisms underlying the mitigation of T cell exhaustion, which may facilitate the development of innovative therapeutic strategies in the field of cancer treatment.

الإتاحة: https://doi.org/10.1186/s13046-023-02888-7Test

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5

دورية أكاديمية

Edible and cation-free kiwi fruit derived vesicles mediated EGFR-targeted siRNA delivery to inhibit multidrug resistant lung cancer

المؤلفون: Huang, Haoying, Yi, Xiaohan, Wei, Qingyun, Li, Mengyuan, Cai, Xueting, Lv, Yan, Weng, Ling, Mao, Yujie, Fan, Weiwei, Zhao, Mengmeng, Weng, Zhongpei, Zhao, Qing, Zhao, Kewei, Cao, Meng, Chen, Jing, Cao, Peng

المساهمون: National Natural Science Foundation of China

المصدر: Journal of Nanobiotechnology ; volume 21, issue 1 ; ISSN 1477-3155

مصطلحات موضوعية: Pharmaceutical Science, Applied Microbiology and Biotechnology, Biomedical Engineering, Molecular Medicine, Medicine (miscellaneous), Bioengineering

الوصف: Clinically, activated EGFR mutation associated chemo-drugs resistance has severely threaten NSCLC patients. Nanoparticle based small interfering RNA (siRNA) therapy representing another promising alternative by silencing specific gene while still suffered from charge associated toxicity, strong immunogenicity and poor targetability. Herein, we reported a novel EGFR-mutant NSCLC therapy relying on edible and cation-free kiwi-derived extracellular vesicles (KEVs), which showed sevenfold enhancement of safe dosage compared with widely used cationic liposomes and could be further loaded with Signal Transducer and Activator of Transcription 3 interfering RNA (siSTAT3). siSTAT3 loaded KEVs (STAT3/KEVs) could be easily endowed with EGFR targeting ability (STAT3/EKEVs) and fluorescence by surface modification with tailor-making aptamer through hydrophobic interaction. STAT3/EKEVs with a controlled size of 186 nm displayed excellent stability, high specificity and good cytotoxicity towards EGFR over-expressing and mutant PC9-GR4-AZD1 cells. Intriguingly, the systemic administration of STAT3/EKEVs significantly suppressed subcutaneous PC9-GR4-AZD1 tumor xenografts in nude mice by STAT3 mediated apoptosis. This safe and robust KEVs has emerged as the next generation of gene delivery platform for NSCLC therapy after multiple drug-resistance. Graphical Abstract

الإتاحة: https://doi.org/10.1186/s12951-023-01766-wTest

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6

دورية أكاديمية

Common Co-activation of AXL and CDCP1 in EGFR-mutation-positive Non-smallcell Lung Cancer Associated With Poor Prognosis.

مصطلحات موضوعية: Animals, Humans, Mice, Carcinoma, Non-Small-Cell Lung, Lung Neoplasms, Disease Models, Animal, Receptor Protein-Tyrosine Kinases, Cell Adhesion Molecules, Neoplasm Proteins, Proto-Oncogene Proteins, RNA, Small Interfering, Antigens, CD, Survival Analysis, Xenograft Model Antitumor Assays, Gene Expression Profiling, Proteomics, Cell Survival, Gene Expression Regulation, Neoplastic, Enzyme Activation, Drug Resistance, Neoplasm, Mutation, Models, Biological, Adult, Aged, Aged, 80 and over, Middle Aged, Female, Male, ErbB Receptors, AXL, CDCP1, Combination therapies, EGFR, Lung cancer, Resistance, and over, Antigens, CD, Carcinoma, Non-Small-Cell Lung, Disease Models, Animal, Drug Resistance, Neoplasm, Gene Expression Regulation, Neoplastic, Models, Biological, RNA, Small Interfering, Clinical Sciences, Public Health and Health Services

الوصف: Epidermal growth factor receptor (EGFR)-mutation-positive non-smallcell lung cancer (NSCLC) is incurable, despite high rates of response to EGFR tyrosine kinase inhibitors (TKIs). We investigated receptor tyrosine kinases (RTKs), Src family kinases and focal adhesion kinase (FAK) as genetic modifiers of innate resistance in EGFR-mutation-positive NSCLC. We performed gene expression analysis in two cohorts (Cohort 1 and Cohort 2) of EGFR-mutation-positive NSCLC patients treated with EGFR TKI. We evaluated the efficacy of gefitinib or osimertinib with the Src/FAK/Janus kinase 2 (JAK2) inhibitor, TPX0005 in vitro and in vivo. In Cohort 1, CUB domain-containing protein-1 (CDCP1) was an independent negative prognostic factor for progression-free survival (hazard ratio of 1.79, p=0.0407) and overall survival (hazard ratio of 2.23, p=0.0192). A two-gene model based on AXL and CDCP1 expression was strongly associated with the clinical outcome to EGFR TKIs, in both cohorts of patients. Our preclinical experiments revealed that several RTKs and non-RTKs, were up-regulated at baseline or after treatment with gefitinib or osimertinib. TPX-0005 plus EGFR TKI suppressed expression and activation of RTKs and downstream signaling intermediates. Co-expression of CDCP1 and AXL is often observed in EGFR-mutation-positive tumors, limiting the efficacy of EGFR TKIs. Co-treatment with EGFR TKI and TPX-0005 warrants testing.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/10n7f0smTest

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7

دورية أكاديمية

Common Co-activation of AXL and CDCP1 in EGFR-mutation-positive Non-Small Cell Lung Cancer Associated With Poor Prognosis

مصطلحات موضوعية: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Women's Health, Genetics, Clinical Research, Lung Cancer, Cancer, Lung, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Adult, Aged, Aged, 80 and over, Animals, Antigens, CD, Antigens, Neoplasm, Carcinoma, Non-Small-Cell Lung, Cell Adhesion Molecules, Cell Survival, Disease Models, Animal, Drug Resistance, Neoplasm, Enzyme Activation, ErbB Receptors, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Lung Neoplasms, Male, Mice, Middle Aged, Models, Biological, Mutation, Neoplasm Proteins, Proteomics, Proto-Oncogene Proteins, RNA, Small Interfering, Receptor Protein-Tyrosine Kinases, Survival Analysis, Xenograft Model Antitumor Assays, Axl Receptor Tyrosine Kinase, Lung cancer, EGFR, Resistance, AXL, CDCP1, Combination therapies, Public Health and Health Services, Clinical sciences, Epidemiology

الوصف: Epidermal growth factor receptor (EGFR)-mutation-positive non-smallcell lung cancer (NSCLC) is incurable, despite high rates of response to EGFR tyrosine kinase inhibitors (TKIs). We investigated receptor tyrosine kinases (RTKs), Src family kinases and focal adhesion kinase (FAK) as genetic modifiers of innate resistance in EGFR-mutation-positive NSCLC. We performed gene expression analysis in two cohorts (Cohort 1 and Cohort 2) of EGFR-mutation-positive NSCLC patients treated with EGFR TKI. We evaluated the efficacy of gefitinib or osimertinib with the Src/FAK/Janus kinase 2 (JAK2) inhibitor, TPX0005 in vitro and in vivo. In Cohort 1, CUB domain-containing protein-1 (CDCP1) was an independent negative prognostic factor for progression-free survival (hazard ratio of 1.79, p=0.0407) and overall survival (hazard ratio of 2.23, p=0.0192). A two-gene model based on AXL and CDCP1 expression was strongly associated with the clinical outcome to EGFR TKIs, in both cohorts of patients. Our preclinical experiments revealed that several RTKs and non-RTKs, were up-regulated at baseline or after treatment with gefitinib or osimertinib. TPX-0005 plus EGFR TKI suppressed expression and activation of RTKs and downstream signaling intermediates. Co-expression of CDCP1 and AXL is often observed in EGFR-mutation-positive tumors, limiting the efficacy of EGFR TKIs. Co-treatment with EGFR TKI and TPX-0005 warrants testing.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/10n7f0smTest
https://escholarship.org/content/qt10n7f0sm/qt10n7f0sm.pdfTest

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8

دورية أكاديمية

Geniposide protects against neurotoxicity in mouse models of rotenone-induced Parkinson's disease involving the mTOR and Nrf2 pathways

المؤلفون: Zhou, Qian, Chen, Bin, Xu, Yijiao, Wang, Yue, He, Ziheng, Cai, Xueting, Qin, Yu, Ye, Juan, Yang, Yang, Shen, Jianping, Cao, Peng

المصدر: Journal of Ethnopharmacology ; volume 318, page 116914 ; ISSN 0378-8741

مصطلحات موضوعية: Drug Discovery, Pharmacology

الإتاحة: https://doi.org/10.1016/j.jep.2023.116914Test
https://api.elsevier.com/content/article/PII:S0378874123007821?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0378874123007821?httpAccept=text/plainTest

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9

دورية أكاديمية

IDH2/R140Q mutation confers cytokine-independent proliferation of TF-1 cells by activating constitutive STAT3/5 phosphorylation.

المؤلفون: Yang, Jie, Chen, Jiao, Chang, Jingjie, Sun, Xiaoyan, Wei, Qingyun, Cai, Xueting, Cao, Peng

المصدر: Cell Communication & Signaling; 2/12/2024, Vol. 22 Issue 1, p1-10, 10p

مصطلحات موضوعية: LEUKEMIA inhibitory factor, CELL proliferation, MACROPHAGE colony-stimulating factor, ONCOSTATIN M, ACUTE myeloid leukemia, ISOCITRATE dehydrogenase, RHINORRHEA

مستخلص: Background: R140Q mutation in isocitrate dehydrogenase 2 (IDH2) promotes leukemogenesis. Targeting IDH2/R140Q yields encouraging therapeutic effects in the clinical setting. However, therapeutic resistance occurs in 12% of IDH2/R140Q inhibitor treated patients. The IDH2/R140Q mutant converted TF-1 cells to proliferate in a cytokine-independent manner. This study investigated the signaling pathways involved in TF-1(R140Q) cell proliferation conversion as alternative therapeutic strategies to improve outcomes in patients with acute myeloid leukemia (AML) harboring IDH2/R140Q. Methods: The effects of IDH2/R140Q mutation on TF-1 cell survival induced by GM-CSF withdrawal were evaluated using flow cytometry assay. The expression levels of apoptosis-related proteins, total or phosphorylated STAT3/5, ERK, and AKT in wild-type TF-1(WT) or TF-1(R140Q) cells under different conditions were evaluated using western blot analysis. Cell viability was tested using MTT assay. The mRNA expression levels of GM-CSF, IL-3, IL-6, G-CSF, leukemia inhibitory factor (LIF), oncostatin M (OSM), and IL-11 in TF-1(WT) and TF-1(R140Q) cells were quantified via RT-PCR. The secretion levels of GM-CSF, OSM, and LIF were determined using ELISA. Results: Our results showed that STAT3 and STAT5 exhibited aberrant constitutive phosphorylation in TF-1(R140Q) cells compared with TF-1(WT) cells. Inhibition of STAT3/5 phosphorylation suppressed the cytokine-independent proliferation of TF-1(R140Q) cells. Moreover, the autocrine GM-CSF, LIF and OSM levels increased, which is consistent with constitutive STAT5/3 activation in TF-1(R140Q) cells, as compared with TF-1(WT) cells. Conclusions: The autocrine cytokines, including GM-CSF, LIF, and OSM, contribute to constitutive STAT3/5 activation in TF-1(R140Q) cells, thereby modulating IDH2/R140Q-mediated malignant proliferation in TF-1 cells. Targeting STAT3/5 phosphorylation may be a novel strategy for the treatment of AML in patients harboring the IDH2/R140Q mutation. BWcAJaJC8rGH42opvAqQCZ Video Abstract [ABSTRACT FROM AUTHOR]

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النص الكامل

10

دورية أكاديمية

Advances in the synergistic and toxic attenuating effect of traditional Chinese medicine in cancer treatment

المؤلفون: CHEN, Jiao, LIN, Dan, YANG, Jie, CAI, XueTing, WEI, GuoLi, CAO, Peng

المصدر: SCIENTIA SINICA Vitae ; volume 52, issue 6, page 920-934 ; ISSN 1674-7232

الإتاحة: https://doi.org/10.1360/ssv-2021-0389Test

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