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21 results on '"Li, Jiang-Chao"'

4. LINC01554-Mediated Glucose Metabolism Reprogramming Suppresses Tumorigenicity in Hepatocellular Carcinoma via Downregulating PKM2 Expression and Inhibiting Akt/mTOR Signaling Pathway

Author

Zheng, Yin-Li, primary, Li, Lei, additional, Jia, Yong-Xun, additional, Zhang, Bao-Zhu, additional, Li, Jiang-Chao, additional, Zhu, Ying-Hui, additional, Li, Meng-Qing, additional, He, Jiao-Zi, additional, Zeng, Ting-Ting, additional, Ban, Xiao-Jiao, additional, Yuan, Yun-Fei, additional, Li, Yan, additional, and Guan, Xin-Yuan, additional

Published
2019
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8. Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway

Author

Zhang, Qian-Qian, primary, Zhou, Da-lei, additional, Lei, Yan, additional, Zheng, Li, additional, Chen, Sheng-Xia, additional, Gou, Hong-Ju, additional, Gu, Qu-Liang, additional, He, Xiao-Dong, additional, Lan, Tian, additional, Qi, Cui-Ling, additional, Li, Jiang-Chao, additional, Ding, Yan-Qing, additional, Qiao, Liang, additional, and Wang, Li-Jing, additional

Published
2014
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9. Andrographolide inhibits melanoma tumor growth by inactivating the TLR4/NF-κB signaling pathway

Author

Zhang, Qian-Qian, primary, Zhou, Da-Lei, additional, Ding, Yi, additional, Liu, Hong-Ying, additional, Lei, Yan, additional, Fang, Hai-Yan, additional, Gu, Qu-Liang, additional, He, Xiao-Dong, additional, Qi, Cui-Ling, additional, Yang, Yi, additional, Lan, Tian, additional, Li, Jiang-Chao, additional, Gong, Ping, additional, Wu, Xiao-Yun, additional, Yang, Xuesong, additional, Li, Wei-Dong, additional, and Wang, Li-Jing, additional

Published
2014
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10. Increased Permeability of the Blood-Brain Barrier and Alzheimer's Disease-Like Alterations in Slit-2 Transgenic Mice

Author

Li, Jiang-chao, primary, Han, Lu, additional, Wen, Yin-xin, additional, Yang, Yong-xia, additional, Li, Shuai, additional, Li, Xue-song, additional, Zhao, Chang-jiang, additional, Wang, Ting-yu, additional, Chen, Hui, additional, Liu, Ying, additional, Qi, Cui-ling, additional, He, Xiao-dong, additional, Gu, Qu-liang, additional, Ye, Yu-xiang, additional, Zhang, Yu, additional, Huang, Ren, additional, Wu, Yu-e, additional, He, Rong-rong, additional, Kurihara, Hiroshi, additional, Song, Xiao-yu, additional, Cao, Liu, additional, and Wang, Li-jing, additional

Published
2014
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16. A novel four-step system for screening angiogenesis inhibitors

Author

ZHOU, QIN, primary, QI, CUI-LING, additional, LI, YAN, additional, HE, XIAO-DONG, additional, LI, JIANG-CHAO, additional, ZHANG, QIAN-QIAN, additional, TIAN, LAN, additional, ZHANG, MING, additional, HAN, ZHE, additional, WANG, HUIPING, additional, YANG, XUESONG, additional, and WANG, LI-JING, additional

Published
2013
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18. Increased Permeability of the Blood-Brain Barrier and Alzheimer's Disease-Like Alterations in Slit-2 Transgenic Mice.

Author

Li, Jiang-chao, Han, Lu, Wen, Yin-xin, Yang, Yong-xia, Li, Shuai, Li, Xue-song, Zhao, Chang-jiang, Wang, Ting-yu, Chen, Hui, Liu, Ying, Qi, Cui-ling, He, Xiao-dong, Gu, Qu-liang, Ye, Yu-xiang, Zhang, Yu, Huang, Ren, Wu, Yu-e, He, Rong-rong, Kurihara, Hiroshi, and Song, Xiao-yu

Subjects
*BLOOD-brain barrier, *ANIMAL models of Alzheimer's disease, *TRANSGENIC mice, *MOLECULAR diagnosis, *APOPTOSIS, *AMYLOID beta-protein, *ACETYLCHOLINESTERASE
Abstract

Alzheimer's disease (AD) is a progressive neurological disorder that primarily affects memory, and its prevalence is rising. Increasing evidence suggests that dysfunction of the blood-brain barrier (BBB) may be involved in AD and other neurodegenerative diseases. Herein, we report that the permeability of the BBB is increased and that AD-like alterations are present in Slit-2 overexpressing transgenic mice. We found that behavioral change and the corresponding molecular diagnostic markers of AD, such as hippocampal neuron apoptosis, amyloid-β (Aβ) protein deposition, and acetylcholinesterase expression, were increased in the Slit-2 transgenic mice. Moreover, the endothelial cells were dysfunctional, the size of the lateral ventricle cavity increased, and the permeability of the BBB increased. Additionally, there was an increased serum level of glutamate indicating that the BBB is related to AD. Finally, histopathological analysis of other organs in the Slit-2 overexpressing mice did not show any marked abnormalities. These findings demonstrate that Slit2 overexpression may be responsible for AD-like alterations and the increased BBB permeability in these mice. Our study provides a potential novel mechanism for the development of AD. [ABSTRACT FROM AUTHOR]

Published
2015
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19. Investigation of Tumor Suppressing Function of CACNA2D3 in Esophageal Squamous Cell Carcinoma.

Author

Li, Yan, Zhu, Cai-Lei, Nie, Chang-Jun, Li, Jiang-Chao, Zeng, Ting-ting, Zhou, Jie, Chen, Jinna, Chen, Kai, Fu, Li, Liu, Haibo, Qin, Yanru, and Guan, Xin-Yuan

Subjects
TUMOR suppressor genes, ESOPHAGEAL cancer, SQUAMOUS cell carcinoma, DELETION mutation, GENE frequency, POLYMERASE chain reaction, GENE expression, CELL migration
Abstract

Background: Deletion of 3p is one of the most frequent genetic alterations in esophageal squamous cell carcinoma (ESCC), suggesting the existence of one or more tumor suppressor genes (TSGs) within these regions. In this study, one TSG, CACNA2D3 at 3p21.1, was characterized. Methods: Expression of CACNA2D3 in ESCCs was tested by quantitative real-time PCR and tissue microarray. The mechanism of CACNA2D3 downregulation was investigated by methylation-specific polymerase chain reaction (MS-PCR). The tumor suppressive function of CACNA2D3 was characterized by both in vitro and in vivo tumorigenic assays, cell migration and invasion assays. Results: CACNA2D3 was frequently downregulated in ESCCs (24/48, 50%), which was significantly associated with promoter methylation and allele loss (P<0.05). Tissue microarray result showed that downregulation of CACNA2D3 was detected in (127/224, 56.7%) ESCCs, which was significantly associated with lymph node metastasis (P = 0.01), TNM staging (P = 0.003) and poor outcome of ESCC patients (P<0.05). Functional studies demonstrated that CACNA2D3 could inhibit tumorigenicity, cell motility and induce apoptosis. Mechanism study found that CACNA2D3 could arrest cell cycle at G1/S checkpoint by increasing expressions of p21 and p53 and decreasing expression of CDK2. In addition, CACNA2D3 could upregulate intracellular free cytosolic Ca2+ and subsequently induce apoptosis. Conclusion: CACNA2D3 is a novel TSG responsible to the 3p21 deletion event and plays a critical suppressing role in the development and progression of ESCC. [ABSTRACT FROM AUTHOR]

Published
2013
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21. Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway.

Author

Zhang QQ, Zhou DL, Lei Y, Zheng L, Chen SX, Gou HJ, Gu QL, He XD, Lan T, Qi CL, Li JC, Ding YQ, Qiao L, and Wang LJ

Subjects
Adenoma genetics, Adenoma pathology, Animals, Carcinoma genetics, Carcinoma pathology, Cell Proliferation, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic metabolism, Cell Transformation, Neoplastic pathology, Colorectal Neoplasms genetics, Colorectal Neoplasms pathology, Disease Models, Animal, Disease Progression, Female, Genes, APC, HCT116 Cells, Humans, Intercellular Signaling Peptides and Proteins genetics, Intestinal Mucosa pathology, Male, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, Nerve Tissue Proteins genetics, RNA Interference, Receptors, Immunologic genetics, Transfection, Tumor Burden, Roundabout Proteins, Adenoma enzymology, Carcinoma enzymology, Colorectal Neoplasms enzymology, Intercellular Signaling Peptides and Proteins metabolism, Intestinal Mucosa enzymology, Nerve Tissue Proteins metabolism, Receptors, Immunologic metabolism, Wnt Signaling Pathway, beta Catenin metabolism, src-Family Kinases metabolism
Abstract

Slit2 is often overexpressed in cancers. Slit2 is a secreted protein that binds to Roundabout (Robo) receptors to regulate cell growth and migration. Here, we employed several complementary mouse models of intestinal cancers, including the Slit2 transgenic mice, the ApcMin/+ spontaneous intestinal adenoma mouse model, and the DMH/DSS-induced colorectal carcinoma model to clarify function of Slit2/Robo1 signaling in intestinal tumorigenesis. We showed that Slit2 and Robo1 are overexpressed in intestinal tumors and may contribute to tumor generation. The Slit2/Robo1 signaling can induce precancerous lesions of the intestine and tumor progression. Ectopic expression of Slit2 activated Slit2/Robo1 signaling and promoted tumorigenesis and tumor growth. This was mediated in part through activation of the Src signaling, which then down-regulated E-cadherin, thereby activating Wnt/β-catenin signaling. Thus, Slit2/Robo1 signaling is oncogenic in intestinal tumorigenesis.

Published
2015
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