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28 results on '"Wang, Tixiao"'

13. TIPE1 promotes liver regeneration by enhancing ROS‐FoxO1 axis mediated autophagy

Author

Zhang, Xiaodong, primary, Li, Shuangjie, additional, Ren, Xiaolei, additional, Xiang, Peng, additional, Zhang, Yankun, additional, Wang, Tixiao, additional, Qin, Qinghua, additional, Sun, Fengkai, additional, Liu, Jingkang, additional, Gao, Lifen, additional, Ma, Chunhong, additional, Yue, Xuetian, additional, Yang, Xiaoyun, additional, Han, Shuang, additional, and Liang, Xiaohong, additional

Published
2022
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14. NAD + salvage governs mitochondrial metabolism, invigorating natural killer cell antitumor immunity

Author

Guo, Xiaowei, primary, Tan, Siyu, additional, Wang, Tixiao, additional, Sun, Renhui, additional, Li, Shuangjie, additional, Tian, Panpan, additional, Li, Mengzhen, additional, Wang, Yuzhen, additional, Zhang, Yankun, additional, Yan, Yuchuan, additional, Dong, Zhaoru, additional, Yan, Lunjie, additional, Yue, Xuetian, additional, Wu, Zhuanchang, additional, Li, Chunyang, additional, Yamagata, Kazuya, additional, Gao, Lifen, additional, Ma, Chunhong, additional, Li, Tao, additional, and Liang, Xiaohong, additional

Published
2022
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15. CD169-positive macrophages enhance abscopal effect of radiofrequency ablation therapy in liver cancer

Author

Song, Xiaojia, primary, Li, Na, additional, Liu, Yuan, additional, Wang, Zehua, additional, Wang, Tixiao, additional, Tan, Siyu, additional, Li, Chunyang, additional, Qiu, Chunhong, additional, Gao, Lifen, additional, Asano, Kenichi, additional, Tanaka, Masato, additional, Liang, Xiaohong, additional, Liu, Xinyong, additional, and Ma, Chunhong, additional

Published
2022
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16. TIPE1 promotes liver regeneration by enhancing ROS‐FoxO1 axis mediated autophagy.

Author

Zhang, Xiaodong, Li, Shuangjie, Ren, Xiaolei, Xiang, Peng, Zhang, Yankun, Wang, Tixiao, Qin, Qinghua, Sun, Fengkai, Liu, Jingkang, Gao, Lifen, Ma, Chunhong, Yue, Xuetian, Yang, Xiaoyun, Han, Shuang, and Liang, Xiaohong

Subjects
LIVER regeneration, LIVER cells, AUTOPHAGY, MICROTUBULE-associated proteins, REACTIVE oxygen species, CARBON tetrachloride
Abstract

The strong regenerative ability of the liver safeguards the crucial hepatic functions. The balance between hepatocyte proliferation and death is critical for restoring liver size and physiology. Tumour necrosis factor (TNF) alpha‐induced protein 8‐like 1 (TIPE1) is highly expressed in liver and has been identified as a candidate regulator for cell proliferation and death, being involved in a variety of biological processes and diseases. However, the role of TIPE1 in liver regeneration remains unexplored. In the present study, we found that TIPE1 expression was elevated in the regenerating liver induced by either partial hepatectomy or 10% carbon tetrachloride administration. Mice with hepatocyte conditional Tipe1 knockout presented significantly impaired liver regeneration. Mechanistically, hepatic Tipe1 deficiency decreased the level of reactive oxygen species in hepatocytes, which in turn led to the inhibition of Forkhead box O1 acetylation and microtubule‐associated protein 1 light chain 3 I to microtubule‐associated protein 1 light chain 3 II conversion, and the accumulation of sequestosome 1. By contrast, forced expression of TIPE1 in hepatocyte significantly promoted liver regeneration following 70% partial hepatectomy and enhanced hepatocyte reactive oxygen species/acetylated‐Forkhead box O1 level and autophagy. These findings indicate that TIPE1 plays a crucial role in liver regeneration by finely regulating the oxidative stress and autophagy and is a potential target for medical intervention of liver regeneration. [ABSTRACT FROM AUTHOR]

Published
2023
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19. ZHX2 inhibits SREBP1c‐mediated de novo lipogenesis in hepatocellular carcinoma via miR‐24‐3p

Author

Yu, Xiangguo, primary, Lin, Qinghai, additional, Wu, Zhuanchang, additional, Zhang, Yankun, additional, Wang, Tixiao, additional, Zhao, Songbai, additional, Song, Xiaojia, additional, Chen, Chaojia, additional, Wang, Zehua, additional, Xu, Leiqi, additional, Li, Chunyang, additional, Gao, Lifen, additional, Liang, Xiaohong, additional, Yue, Xuetian, additional, and Ma, Chunhong, additional

Published
2020
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20. Zhx2 Accelerates Sepsis by Promoting Macrophage Glycolysis via Pfkfb3

Author

Wang, Zehua, primary, Kong, Liang, additional, Tan, Siyu, additional, Zhang, Yankun, additional, Song, Xiaojia, additional, Wang, Tixiao, additional, Lin, Qinghai, additional, Wu, Zhuanchang, additional, Xiang, Peng, additional, Li, Chunyang, additional, Gao, Lifen, additional, Liang, Xiaohong, additional, and Ma, Chunhong, additional

Published
2020
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21. Tim-3 Hampers Tumor Surveillance of Liver-Resident and Conventional NK Cells by Disrupting PI3K Signaling

Author

Tan, Siyu, primary, Xu, Yong, additional, Wang, Zehua, additional, Wang, Tixiao, additional, Du, Xianhong, additional, Song, Xiaojia, additional, Guo, Xiaowei, additional, Peng, Jiali, additional, Zhang, Jie, additional, Liang, Yan, additional, Lu, Jinghui, additional, Peng, Jun, additional, Gao, Chengjiang, additional, Wu, Zhuanchang, additional, Li, Chunyang, additional, Li, Nailin, additional, Gao, Lifen, additional, Liang, Xiaohong, additional, and Ma, Chunhong, additional

Published
2020
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22. ZHX2 restricts hepatocellular carcinoma by suppressing stem cell-like traits through KDM2A-mediated H3K36 demethylation

Author

Lin, Qinghai, primary, Wu, Zhuanchang, additional, Yue, Xuetian, additional, Yu, Xiangguo, additional, Wang, Zehua, additional, Song, Xiaojia, additional, Xu, Leiqi, additional, He, Ying, additional, Ge, Yutong, additional, Tan, Siyu, additional, Wang, Tixiao, additional, Song, Hui, additional, Yuan, Detian, additional, Gong, Yaoqin, additional, Gao, Lifen, additional, Liang, Xiaohong, additional, and Ma, Chunhong, additional

Published
2020
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23. Soluble Tim-3 serves as a tumor prognostic marker and therapeutic target for CD8+T cell exhaustion and anti-PD-1 resistance

Author

Chen, Chaojia, Zhao, Fangcheng, Peng, Jiali, Zhao, Di, Xu, Liyun, Li, Huayu, Ma, Shuaiya, Peng, Xueqi, Sheng, Xue, Sun, Yang, Wang, Tixiao, Dong, Haoqing, Ding, Yuming, Wu, Zhuanchang, Liang, Xiaohong, Gao, Lifen, Wang, Hongyan, Ma, Chunhong, and Li, Chunyang

Abstract

Resistance to PD-1 blockade in onco-immunotherapy greatly limits its clinical application. T cell immunoglobulin and mucin domain containing-3 (Tim-3), a promising immune checkpoint target, is cleaved by ADAM10/17 to produce its soluble form (sTim-3) in humans, potentially becoming involved in anti-PD-1 resistance. Herein, serum sTim-3 upregulation was observed in non-small cell lung cancer (NSCLC) and various digestive tumors. Notably, serum sTim-3 is further upregulated in non-responding patients undergoing anti-PD-1 therapy for NSCLC and anti-PD-1-resistant cholangiocarcinoma patients. Furthermore, sTim-3 overexpression facilitates tumor progression and confers anti-PD-1 resistance in multiple tumor mouse models. Mechanistically, sTim-3 induces terminal T cell exhaustion and attenuates CD8+T cell response to PD-1 blockade through carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1). Moreover, the ADAM10 inhibitor GI254023X, which blocks sTim-3 production, reduces tumor progression in Tim-3 humanized mice and reverses anti-PD-1 resistance in human tumor-infiltrating lymphocytes (TILs). Overall, human sTim-3 holds great predictive and therapeutic potential in onco-immunotherapy.

Published
2024
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24. ZHX2 Restricts Hepatocellular Carcinoma by Suppressing Stem Cell-Like Traits Through KDM2A-Mediated H3K36 Demethylation

Author

Lin, Qinghai, primary, Wu, Zhuanchang, additional, Yue, Xuetian, additional, Yu, Xiangguo, additional, Wang, Zehua, additional, Song, Xiaojia, additional, Xu, Leiqi, additional, He, Ying, additional, Ge, Yutong, additional, Tan, Siyu, additional, Wang, Tixiao, additional, Yuan, Detian, additional, Gong, Yaoqing, additional, Gao, Lifen, additional, Liang, Xiaohong, additional, and Ma, chunhong, additional

Published
2019
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28. NAD + salvage governs mitochondrial metabolism, invigorating natural killer cell antitumor immunity.

Author

Guo X, Tan S, Wang T, Sun R, Li S, Tian P, Li M, Wang Y, Zhang Y, Yan Y, Dong Z, Yan L, Yue X, Wu Z, Li C, Yamagata K, Gao L, Ma C, Li T, and Liang X

Subjects
Humans, Mice, Animals, NAD metabolism, Nicotinamide Mononucleotide metabolism, Cytokines metabolism, Killer Cells, Natural metabolism, Tumor Microenvironment, Carcinoma, Hepatocellular, Liver Neoplasms
Abstract

Background and Aims: Natural killer (NK) cells are key players in tumor immunosurveillance, and metabolic adaptation manipulates their fate and functional state. The nicotinamide adenine dinucleotide (NAD + ) has emerged as a vital factor to link cellular metabolism and signaling transduction. Here, we identified NAD + metabolism as a central hub to determine the homeostasis and function of NK cells., Approach and Results: NAD + level was elevated in activated NK cells. NAD + supplementation not only enhanced cytokine production and cytotoxicity but also improved the proliferation and viability of NK cells. Intriguingly, the salvage pathway was involved in maintaining NAD + homeostasis in activated NK cells. Genetic ablation or pharmacological blockade of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD + salvage pathway, markedly destroyed the viability and function of NK cells. Mechanistically, NAD + salvage dictated the mitochondrial homeostasis and oxidative phosphorylation activity to support the optimal function of NK cells. However, in human HCC tissues, NAMPT expression and NAD + level were significantly down-regulated in tumor-infiltrating NK cells, which negatively correlated with patient survival. And lactate accumulation in the tumor microenvironment was at least partially responsible for the transcriptional repression of NAMPT in NK cells. Further, deficiency of Nampt in NK cells accelerated the growth of HCC and melanoma. Supplementation of the NAD + precursor nicotinamide mononucleotide (NMN) significantly improved NK antitumor response in both mouse and human cell-derived xenografts., Conclusions: These findings reveal NAD + salvage as an essential factor for NK-cell homeostasis and function, suggesting a potential strategy for invigorating NK cell-based immunotherapy., (Copyright © 2023 American Association for the Study of Liver Diseases.)

Published
2023
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