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Your search keyword '"Dai, Xinzheng"' showing total 31 results
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31 results on '"Dai, Xinzheng"'

7. Hepatocyte deubiquitinating enzyme OTUD5 deficiency is a key aggravator for metabolic dysfunction-associated steatohepatitis by disturbing mitochondrial homeostasis

Author

Dai, Jingjing, primary, Zhang, Liren, additional, Zhang, Ruizhi, additional, Ge, Jing, additional, Yao, Feifan, additional, Zhou, Suiqing, additional, Xu, Jiali, additional, Yu, Kai, additional, Xu, Jing, additional, Jiang, Longfeng, additional, Jin, Ke, additional, Dai, Xinzheng, additional, Li, Jun, additional, and Li, Qing, additional

Published
2023
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8. Endothelial DGKG promotes tumor angiogenesis and immune evasion in hepatocellular carcinoma

Author

Zhang, Liren, primary, Xu, Jiali, additional, Zhou, Suiqing, additional, Yao, Feifan, additional, Zhang, Ruizhi, additional, You, Wenhua, additional, Yu, Kai, additional, Zhang, Yu, additional, Baheti, Tasiken, additional, Pu, Liyong, additional, Xu, Jing, additional, Qian, Xiaofeng, additional, Xia, Yongxiang, additional, Dai, Xinzheng, additional, Li, Qing, additional, and Wang, Xuehao, additional

Published
2023
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10. Emerging mechanisms progress of colorectal cancer liver metastasis

Author

Zhao, Wenhu, Dai, Shipeng, Yue, Lei, Xu, Fan, Gu, Jian, Dai, Xinzheng, and Qian, Xiaofeng

Subjects
Endocrinology, Diabetes and Metabolism, Liver Neoplasms, Humans, Colorectal Neoplasms
Abstract

Colorectal cancer (CRC) is the third most common malignancy and the second most common cause of cancer-related mortality worldwide. A total of 20% of CRC patients present with distant metastasis. The hepatic portal venous system, responsible for collecting most intestinal blood, makes the liver the most common site of CRC metastasis. The formation of liver metastases from colorectal cancer is a long and complex process. It involves the maintenance of primary tumors, vasculature invasion, distant colonization, and metastasis formation. In this review, we serve on how the CRC cells acquire stemness, invade the vascular, and colonize the liver. In addition, we highlight how the resident cells of the liver and immune cells interact with CRC cells. We also discuss the current immunotherapy approaches and challenges we face, and finally, we look forward to finding new therapeutic targets based on novel sequencing technologies.

Published
2022
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11. Safety and Efficacy of Sintilimab and Anlotinib as First Line Treatment for Advanced Hepatocellular Carcinoma (KEEP-G04): A Single-Arm Phase 2 Study

Author

Chen, Xiaofeng, primary, Li, Wei, additional, Wu, Xiaofeng, additional, Zhao, Fengjiao, additional, Wang, Deqiang, additional, Wu, Hao, additional, Gu, Yanhong, additional, Li, Xiao, additional, Qian, Xiaofeng, additional, Hu, Jun, additional, Li, Changxian, additional, Xia, Yongxiang, additional, Rao, Jianhua, additional, Dai, Xinzheng, additional, Shao, Qianwen, additional, Tang, Jie, additional, Li, Xiangcheng, additional, and Shu, Yongqian, additional

Published
2022
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19. Hypomethylation‐mediated activation of cancer/testis antigen KK‐LC‐1 facilitates hepatocellular carcinoma progression through activating the Notch1/Hes1 signalling

Author

Chen, Zhiqiang, primary, Zuo, Xueliang, additional, Pu, Liyong, additional, Zhang, Yao, additional, Han, Guoyong, additional, Zhang, Long, additional, Wu, Zhengshan, additional, You, Wei, additional, Qin, Jianjie, additional, Dai, Xinzheng, additional, Shen, Hongbing, additional, Wang, Xuehao, additional, and Wu, Jindao, additional

Published
2019
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20. 5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

Author

Zuo, Xueliang, primary, Chen, Zhiqiang, additional, Cai, Juan, additional, Gao, Wen, additional, Zhang, Yao, additional, Han, Guoyong, additional, Pu, Liyong, additional, Wu, Zhengshan, additional, You, Wei, additional, Qin, Jianjie, additional, Dai, Xinzheng, additional, Shen, Hongbing, additional, Wu, Jindao, additional, and Wang, Xuehao, additional

Published
2019
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24. Enhanced in vitro and in vivo therapeutic efficacy of codrug-loaded nanoparticles against liver cancer

Author

Li,Xiaolin, Xu,Hua’e, Dai,Xinzheng, Zhu ,Zhenshu, Liu,Baorui, Liu,Xiaowei, Li,Xiaolin, Xu,Hua’e, Dai,Xinzheng, Zhu ,Zhenshu, Liu,Baorui, and Liu,Xiaowei

Abstract

Xiaolin Li,1,* Hua’e Xu,2,* Xinzheng Dai,3,4,* Zhenshu Zhu,5 Baorui Liu,6 Xiaowei Lu11Department of Geriatrics, 2Department of Pharmacy, the First Affiliated Hospital to Nanjing Medical University, Nanjing; 3Key Laboratory of Living Donor Liver Transplantation, Ministry of Public Health, 4Liver Transplantation Center, the First Affiliated Hospital to Nanjing Medical University, Nanjing; 5Department of Pharmaceutical Analysis, China Pharmaceutical University, Nanjing; 6The Comprehensive Cancer Center of Drum Tower Hospital, Medical School of Nanjing University and Clinical Cancer Institute of Nanjing University, Nanjing, China*These authors contributed equally to this workAbstract: Paclitaxel (Ptx), one of the most widely used anticancer agents, has demonstrated extraordinary activities against a variety of solid tumors. However, the therapeutic response of Ptx is often associated with severe side effects caused by its nonspecific cytotoxic effects and special solvents (Cremophor EL®). The current study reports the stable controlled release of Ptx/tetrandrine (Tet)-coloaded nanoparticles by amphilic methoxy poly(ethylene glycol)–poly(caprolactone) block copolymers. There were three significant findings. Firstly, Tet could effectively stabilize Ptx-loaded nanoparticles with the coencapsulation of Tet and Ptx. The influence of different Ptx/Tet feeding ratios on the size and loading efficiency of the nanoparticles was also explored. Secondly, the encapsulation of Tet and Ptx into nanoparticles retains the synergistic anticancer efficiency of Tet and Ptx against mice hepatoma H22 cells. Thirdly, in the in vivo evaluation, intratumoral administration was adopted to increase the site-specific delivery. Ptx/Tet nanoparticles, when delivered intratumorally, exhibited significantly improved antitumor efficacy; moreover, they substantially increased the overall survival in an established H22-transplanted mice model. Further investigation into the a

Published
2012

29. Short-term starvation attenuates liver ischemia-reperfusion injury (IRI) by Sirt1-autophagy signaling in mice.

Author

Qin J, Zhou J, Dai X, Zhou H, Pan X, Wang X, Zhang F, Rao J, and Lu L

Abstract

Calorie restriction or starvation (fasting) has some beneficial effects in terms of prolonging life and increasing resistance to stress. It has also been shown that calorie restriction has a protective role during ischemia-reperfusion injury (IRI) in several organs, but the underlying mechanism has not been elucidated. In this study we investigated the effects and molecular mechanisms of short-term starvation (STS) on liver IRI in a mouse liver IRI model. We found that STS significantly attenuated liver IRI in this model, as evidenced by inhibition of serum aminotransferase levels, and decreased pathological damage and hepatocellular apoptosis, especially after 2- or 3-day starvation. Furthermore, we found that 2- or 3-day starvation induced expression of hepatocellular autophagy in vivo and in vitro. Further experiments provided support for the notion that STS-induced autophagy played a key role during starvation-regulated protection against liver IRI via autophagy inhibition with 3-methyladenine. Interestingly, the longevity gene Sirt1 was also significantly up-regulated in liver after STS. Importantly, inhibition of Sirt1 by sirtinol abolished STS-induced autophagy and further abrogated STS-mediated protection against liver IRI. In conclusion, our results indicate that STS attenuates liver IRI via the Sirt1-autophagy pathway. Our findings provide a rationale for a novel therapeutic strategy for managing liver IRI.

Published
2016

30. OCT4 regulates epithelial-mesenchymal transition and its knockdown inhibits colorectal cancer cell migration and invasion.

Author

Dai X, Ge J, Wang X, Qian X, Zhang C, and Li X

Subjects
Animals, Apoptosis, Biomarkers, Tumor genetics, Blotting, Western, Cell Adhesion, Cell Proliferation, Colorectal Neoplasms genetics, Colorectal Neoplasms metabolism, Female, Fluorescent Antibody Technique, Humans, Immunoenzyme Techniques, Liver Neoplasms genetics, Liver Neoplasms metabolism, Mice, Mice, Nude, Neoplasm Invasiveness, Neoplasm Staging, Octamer Transcription Factor-3 antagonists & inhibitors, Octamer Transcription Factor-3 genetics, Prognosis, RNA, Messenger genetics, RNA, Small Interfering genetics, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Tumor Cells, Cultured, Biomarkers, Tumor metabolism, Cell Movement, Colorectal Neoplasms pathology, Epithelial-Mesenchymal Transition, Liver Neoplasms secondary, Octamer Transcription Factor-3 metabolism
Abstract

Octamer-binding transcription factor 4 (OCT4) has been implicated in cancer metastasis. In this study, we investigated whether OCT4 promotes colorectal cancer (CRC) metastasis through the epithelial-mesenchymal transition (EMT) process. We designed our experiment as a loss-of-function study. Western blot analysis was used to measure the extent and stability of OCT4 knockdown. We evaluated the metastatic phenotype of OCT4-silenced SW620 cells using standard migration and invasion assays in vitro and the commonly used mouse model for experimental metastases in vivo. We found that OCT4 knockdown inhibited colorectal cancer cell motility and invasion (in vitro) and decreased hepatic colonization (in vivo). It also induced changes in EMT characteristic cell morphology and marker gene expression. In addition, its knockdown decreased WNT pathway activity. Finally, in human primary colorectal cancers, the frequency of upregulated OCT4 expression in cases with liver metastasis was statistically higher than that in cases without liver metastasis. These results indicate that OCT4 may contribute to CRC cell metastasis through EMT and serves as a promising biomarker for identifying CRC patients at high risk for liver metastases.

Published
2013
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31. Enhanced in vitro and in vivo therapeutic efficacy of codrug-loaded nanoparticles against liver cancer.

Author

Li X, Xu H, Dai X, Zhu Z, Liu B, and Lu X

Subjects
Animals, Antineoplastic Agents administration & dosage, Antineoplastic Agents chemistry, Antineoplastic Combined Chemotherapy Protocols chemistry, Benzylisoquinolines chemistry, Carcinoma, Hepatocellular pathology, Cell Line, Tumor, Drug Synergism, Mice, Nanocapsules administration & dosage, Paclitaxel chemistry, Survival Analysis, Survival Rate, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols administration & dosage, Benzylisoquinolines administration & dosage, Carcinoma, Hepatocellular drug therapy, Delayed-Action Preparations administration & dosage, Delayed-Action Preparations chemical synthesis, Nanocapsules chemistry, Paclitaxel administration & dosage
Abstract

Paclitaxel (Ptx), one of the most widely used anticancer agents, has demonstrated extraordinary activities against a variety of solid tumors. However, the therapeutic response of Ptx is often associated with severe side effects caused by its nonspecific cytotoxic effects and special solvents (Cremophor EL(®)). The current study reports the stable controlled release of Ptx/tetrandrine (Tet)-coloaded nanoparticles by amphilic methoxy poly(ethylene glycol)-poly(caprolactone) block copolymers. There were three significant findings. Firstly, Tet could effectively stabilize Ptx-loaded nanoparticles with the coencapsulation of Tet and Ptx. The influence of different Ptx/Tet feeding ratios on the size and loading efficiency of the nanoparticles was also explored. Secondly, the encapsulation of Tet and Ptx into nanoparticles retains the synergistic anticancer efficiency of Tet and Ptx against mice hepatoma H22 cells. Thirdly, in the in vivo evaluation, intratumoral administration was adopted to increase the site-specific delivery. Ptx/Tet nanoparticles, when delivered intratumorally, exhibited significantly improved antitumor efficacy; moreover, they substantially increased the overall survival in an established H22-transplanted mice model. Further investigation into the anticancer mechanisms of this nanodelivery system is under active consideration as a part of this ongoing research. The results suggest that Ptx/Tet-coloaded nanoparticles could be a potential useful chemotherapeutic formulation for liver cancer therapy.

Published
2012
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