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25 results on '"Wang, Chia-Jen"'

4. Validation of bioactive components from traditional Chinese medicine for lifespan extension

Author

Chen, Chin-Chuan, primary, Wang, Tong-Hong, additional, Tseng, Wei-Che, additional, Leu, Yann-Lii, additional, Chen, Chi-Yuan, additional, Lee, Wen-Chih, additional, Chi, Ying-Chih, additional, Cheng, Shu-Fang, additional, Lai, Chun-Yu, additional, Kuo, Cheng-Hsin, additional, Yang, Shu-Ling, additional, Shen, Jiann-Jong, additional, Yang, Sien-Hung, additional, Feng, Chun-Hao, additional, Wu, Chih-Ching, additional, Hwang, Tsong-Long, additional, Wang, Chia-Jen, additional, and Wang, Shu-Huei, additional

Published
2021
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6. Suppression of Drug-Resistant Non-Small-Cell Lung Cancer with Inhibitors Targeting Minichromosomal Maintenance Protein

Author

Lin, Chia-Yi, primary, Wu, Hsin-Yi, additional, Hsu, Yuan-Ling, additional, Cheng, Ting-Jen Rachel, additional, Liu, Jyung-Hurng, additional, Huang, Rou-Jie, additional, Hsiao, Tzu-Hung, additional, Wang, Chia-Jen, additional, Hung, Pei-Fang, additional, Lan, Albert, additional, Pan, Szu-Hua, additional, Chein, Rong-Jie, additional, Wong, Chi-Huey, additional, and Yang, Pan-Chyr, additional

Published
2020
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10. Protective role of programmed death 1 ligand 1 (PD-L1) in nonobese diabetic mice: the paradox in transgenic models

Author

Wang, Chia-Jen, Chou, Feng-Cheng, Chu, Chi-Hong, Wu, Jen-Chine, Lin, Shih-Hua, Chang, Deh-Ming, and Sytwu, Huey-Kang

Subjects
Ligands (Biochemistry) -- Research -- Usage -- Physiological aspects, Diabetes -- Research -- Physiological aspects, Lymphocytes -- Research -- Physiological aspects -- Usage, Animal models in research -- Usage -- Research -- Physiological aspects, Health, Usage, Physiological aspects, Research
Abstract

OBJECTIVE--Coinhibitory signals mediated via programmed death 1 (PD-1) receptor play a critical role in downregulating immune responses and in maintaining peripheral tolerance. Programmed death 1 ligand 1 (PD-L1), the interacting ligand for PD-1, widely expressed in many cell types, acts as a tissue-specific negative regulator of pathogenic T-cell responses. We investigated the protective potential of PD-L1 on autoimmune diabetes by transgenically overexpressing PD-L1 in pancreatic p-cells in nonobese diabetic (NOD) mice. RESEARCH DESIGN AND METHODS--We established an insulin promoter-driven murine PD-L1 transgenic NOD mouse model to directly evaluate the protective effect of an organ-specific PD-L1 transgene against autoimmune diabetes. Transgene expression, insulitis, and diabetic incidence were characterized in these transgenic NOD mice. Lymphocyte development, Th1 cells, and regulatory T-cells were analyzed in these transgenic mice; and T-cell proliferation, adoptive transfer, and islet transplantation were performed to evaluate the PD-L1 transgene-mediated immuneprotective mechanisms. RESULTS--The severity of insulitis in these transgenic mice is significantly decreased, disease onset is delayed, and the incidence of diabetes is markedly decreased compared with littermate controls. NOD/SCID mice that received lymphocytes from transgenic mice became diabetic at a slower rate than mice receiving control lymphocytes. Moreover, lymphocytes collected from recipients transferred by lymphocytes from transgenic mice revealed less proliferative potential than lymphocytes obtained from control recipients. Transgenic islets transplanted in diabetic recipients survived moderately longer than control islets. CONCLUSIONS--Our results demonstrate the protective potential of transgenic PD-L1 in autoimmune diabetes and illustrate its role in downregulating diabetogenic T-cells in NOD mice. Diabetes 57:1861-1869, 2008, Programmed death 1 (PD-1) is an immunoreceptor of the CD28/CTLA-4 family whose expression is induced in activated T- and B-cells and in macrophages (1,2). PD-1 has two cytoplasmic tyrosine motifs: [...]

Published
2008

11. 2-anilino-4-amino-5-aroylthiazole-type compound AS7128 inhibits lung cancer growth through decreased iASPP and p53 interaction

Author

Cheng, Hao-Wei, primary, Chein, Rong-Jie, additional, Cheng, Ting-Jen, additional, Wu, Pei-Shan, additional, Wu, Hsin-Yi, additional, Hung, Pei-Fang, additional, Wang, Chia-Jen, additional, Hsu, Yuan-Ling, additional, Wong, Jau-Min, additional, Yuan, Ang, additional, Wong, Chi-Huey, additional, Yang, Pan-Chyr, additional, and Pan, Szu-Hua, additional

Published
2018
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13. Purine-Type Compounds Induce Microtubule Fragmentation and Lung Cancer Cell Death through Interaction with Katanin

Author

Kuo, Ting-Chun, primary, Li, Ling-Wei, additional, Pan, Szu-Hua, additional, Fang, Jim-Min, additional, Liu, Jyung-Hurng, additional, Cheng, Ting-Jen, additional, Wang, Chia-Jen, additional, Hung, Pei-Fang, additional, Chen, Hsuan-Yu, additional, Hong, Tse-Ming, additional, Hsu, Yuan-Ling, additional, Wong, Chi-Huey, additional, and Yang, Pan-Chyr, additional

Published
2016
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23. Shisa3 Is Associated with Prolonged Survival through Promoting [beta]-Catenin Degradation in Lung Cancer.

Author

Chen, Chun-Chieh, Chen, Hsuan-Yu, Su, Kang-Yi, Hong, Qi-Sheng, Yan, Bo-Shiun, Chen, Ching-Hsien, Pan, Szu-Hua, Chang, Yih-Leong, Wang, Chia-Jen, Hung, Pei-Fang, Yuan, Shinsheng, Chang, Gee-Chen, Chen, Jeremy J W, Yang, Pan-Chyr, Yang, Ya-Chien, and Yu, Sung-Liang

Abstract

RATIONALE: Despite advances in treatment and prognosis of non-small cell lung cancer (NSCLC), patient outcomes are still unsatisfactory. OBJECTIVES: To reduce the morbidity and mortality of patients with NSCLC, a more comprehensive understanding of mechanisms involved in cancer progression is urgently needed. METHODS: By comparison of gene expression profiles in the cell line pair with differential invasion ability, CL1-0 and CL1-5, we found that Shisa3 was highly expressed in the low invasive cells. The effect of Shisa3 on invasion, migration, proliferation, apoptosis, epithelial-mesenchymal transition, and anchorage-independent growth activities in vitro and on tumor growth and metastasis in mice models were examined. The underlying mechanism of Shisa3 was explored by microarray and pathway analysis. Finally, the correlation of Shisa3 expression and clinical outcome was also calculated. MEASUREMENTS AND MAIN RESULTS: We identified Shisa3 as a novel tumor suppressor, which induces [beta]-catenin degradation resulting in suppression of tumorigenesis and invasion in vitro. Shisa3 decreased the tumor growth in mice with subcutaneous implantation and reduced the number of metastatic nodules in mice with tail vein injection and orthotopic implantation. Shisa3 performs the tumor suppression activity through WNT signaling predicted by microarray analysis. Our data found that Shisa3 accelerates [beta]-catenin degradation and was positively associated with overall survival and progression-free survival of NSCLC. CONCLUSIONS: Our results reveal that Shisa3 acts as a tumor suppressor by acceleration of [beta]-catenin degradation and provide new insight for cancer prognosis and therapy. [ABSTRACT FROM AUTHOR]

Published
2014
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