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32 results on '"Sun, Qi-Man"'

4. Macro CD5L+ deteriorates CD8+T cells exhaustion and impairs combination of Gemcitabine-Oxaliplatin-Lenvatinib-anti-PD1 therapy in intrahepatic cholangiocarcinoma

Author

Lu, Jia-Cheng, primary, Wu, Lei-Lei, additional, Sun, Yi-Ning, additional, Huang, Xiao-Yong, additional, Gao, Chao, additional, Guo, Xiao-Jun, additional, Zeng, Hai-Ying, additional, Qu, Xu-Dong, additional, Chen, Yi, additional, Wu, Dong, additional, Pei, Yan-Zi, additional, Meng, Xian-Long, additional, Zheng, Yi-Min, additional, Liang, Chen, additional, Zhang, Peng-Fei, additional, Cai, Jia-Bin, additional, Ding, Zhen-Bin, additional, Yang, Guo-Huan, additional, Ren, Ning, additional, Huang, Cheng, additional, Wang, Xiao-Ying, additional, Gao, Qiang, additional, Sun, Qi-Man, additional, Shi, Ying-Hong, additional, Qiu, Shuang-Jian, additional, Ke, Ai-Wu, additional, Shi, Guo-Ming, additional, Zhou, Jian, additional, Sun, Yi-Di, additional, and Fan, Jia, additional

Published
2024
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6. Application of a Single-Cell-RNA-Based Biological-Plausible Graph Neural Network in Diagnosis of Primary Liver Tumours

Author

Zhang, Dao-Han, primary, Liang, Chen, additional, Huang, Xiao-Yong, additional, Yu, Lei, additional, Meng, Xianlong, additional, Guo, Xiao-Jun, additional, Zeng, Hai-Ying, additional, Chen, Zhen, additional, Zhang, Lv, additional, Pei, Yanzi, additional, Hu, Shu-Yang, additional, Ye, Mu, additional, Cai, Jiabin, additional, Huang, Pei-Xin, additional, Shi, Ying-Hong, additional, Ke, Aiwu, additional, Chen, Yi, additional, Ji, Yuan, additional, Shi, Yujiang Geno, additional, Zhou, Jian, additional, Fan, Jia, additional, Yang, Guo-Huang, additional, Sun, Qi-Man, additional, Shi, Guo-Ming, additional, and Lu, Jia-Cheng, additional

Published
2023
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7. The clinical implications and molecular features of intrahepatic cholangiocarcinoma with perineural invasion

Author

Meng, Xian-Long, primary, Lu, Jia-Cheng, additional, Zeng, Hai-Ying, additional, Chen, Zhen, additional, Guo, Xiao-Jun, additional, Gao, Chao, additional, Pei, Yan-Zi, additional, Hu, Shu-Yang, additional, Ye, Mu, additional, Sun, Qi-Man, additional, Yang, Guo-Huang, additional, Cai, Jia-Bin, additional, Huang, Pei-Xin, additional, Yv, Lei, additional, Zhang, Lv, additional, Shi, Ying-Hong, additional, Ke, Ai-Wu, additional, Zhou, Jian, additional, Fan, Jia, additional, Chen, Yi, additional, Huang, Xiao-Yong, additional, and Shi, Guo-Ming, additional

Published
2022
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9. CTLA-4 Synergizes With PD1/PD-L1 in the Inhibitory Tumor Microenvironment of Intrahepatic Cholangiocarcinoma

Author

Guo, Xiao-Jun, primary, Lu, Jia-Cheng, additional, Zeng, Hai-Ying, additional, Zhou, Rong, additional, Sun, Qi-Man, additional, Yang, Guo-Huan, additional, Pei, Yan-Zi, additional, Meng, Xian-Long, additional, Shen, Ying-Hao, additional, Zhang, Peng-Fei, additional, Cai, Jia-Bin, additional, Huang, Pei-Xin, additional, Ke, Ai-Wu, additional, Shi, Ying-Hong, additional, Zhou, Jian, additional, Fan, Jia, additional, Chen, Yi, additional, Yang, Liu-Xiao, additional, Shi, Guo-Ming, additional, and Huang, Xiao-Yong, additional

Published
2021
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13. Plasma MicroRNA Panel Predicts Early Tumor Recurrence in Patients with Hepatocellular Carcinoma after Liver Transplantation

Author

Huang, Ao, primary, Guo, De-Zhen, additional, Wang, Yu-Peng, additional, Yang, Guo-Huan, additional, Sun, Qi-Man, additional, Zhang, Xin, additional, He, Yi-Feng, additional, Song, Kang, additional, Huang, Xiao-Wu, additional, Yang, Xin-Rong, additional, Fan, Jia, additional, Zhou, Jian, additional, and Hu, Jie, additional

Published
2021
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14. Graft Programmed Death Ligand 1 Expression as a Marker for Transplant Rejection Following Anti–Programmed Death 1 Immunotherapy for Recurrent Liver Tumors

Author

Shi, Guo‐Ming, primary, Wang, Jiping, additional, Huang, Xiao‐Wu, additional, Huang, Xiao‐Yong, additional, He, Yi‐Feng, additional, Ji, Yuan, additional, Chen, Yi, additional, Wu, Dong, additional, Lu, Jia‐Cheng, additional, Sun, Qi‐Man, additional, Liu, Wei‐Ren, additional, Wang, Ting, additional, Yang, Liu‐Xiao, additional, Hou, Ying‐Yong, additional, Shi, Ying‐Hong, additional, Sun, Jian, additional, Xiao, Yong‐Sheng, additional, Wang, Zheng, additional, Fan, Jia, additional, Bertagnolli, Monica M., additional, and Zhou, Jian, additional

Published
2020
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17. Graft Programmed Death Ligand 1 Expression as a Marker for Transplant Rejection Following Anti–Programmed Death 1 Immunotherapy for Recurrent Liver Tumors.

Author

Shi, Guo‐Ming, Wang, Jiping, Huang, Xiao‐Wu, Huang, Xiao‐Yong, He, Yi‐Feng, Ji, Yuan, Chen, Yi, Wu, Dong, Lu, Jia‐Cheng, Sun, Qi‐Man, Liu, Wei‐Ren, Wang, Ting, Yang, Liu‐Xiao, Hou, Ying‐Yong, Shi, Ying‐Hong, Sun, Jian, Xiao, Yong‐Sheng, Wang, Zheng, Fan, Jia, and Bertagnolli, Monica M.

Published
2021
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18. Distinct PD-L1/PD1 Profiles and Clinical Implications in Intrahepatic Cholangiocarcinoma Patients with Different Risk Factors

Author

Lu, Jia-Cheng, primary, Zeng, Hai-Ying, additional, Sun, Qi-Man, additional, Meng, Qing-Nan, additional, Huang, Xiao-Yong, additional, Zhang, Peng-Fei, additional, Yang, Xuan, additional, Peng, Rui, additional, Gao, Chao, additional, Wei, Chuan-Yuan, additional, Shen, Ying-Hao, additional, Cai, Jia-Bing, additional, Dong, Rui-Zhao, additional, Shi, Ying-Hong, additional, Sun, Hui-Chuan, additional, Shi, Yujiang G., additional, Zhou, Jian, additional, Fan, Jia, additional, Ke, Ai-Wu, additional, Yang, Liu-Xiao, additional, and Shi, Guo-Ming, additional

Published
2019
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19. Long non-coding RNA 00607 as a tumor suppressor by modulating NF-κB p65/p53 signaling axis in hepatocellular carcinoma

Author

Sun, Qi-Man, primary, Hu, Bo, additional, Fu, Pei-Yao, additional, Tang, Wei-Guo, additional, Zhang, Xin, additional, Zhan, Hao, additional, Sun, Chao, additional, He, Yi-Feng, additional, Song, Kang, additional, Xiao, Yong-Sheng, additional, Sun, Jian, additional, Xu, Yang, additional, Zhou, Jian, additional, and Fan, Jia, additional

Published
2018
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20. Corrigendum to “Circumventing intratumoral heterogeneity to identify potential therapeutic targets in hepatocellular carcinoma” [J Hepatol 67 (2017) 293–301]

Author

Huang, Ao, primary, Zhao, Xin, additional, Yang, Xin-Rong, additional, Li, Fu-Qiang, additional, Zhou, Xin-Lan, additional, Wu, Kui, additional, Zhang, Xin, additional, Sun, Qi-Man, additional, Cao, Ya, additional, Zhu, Hong-Mei, additional, Wang, Xiang-Dong, additional, Yang, Huan-Ming, additional, Wang, Jian, additional, Tang, Zhao-You, additional, Hou, Yong, additional, Fan, Jia, additional, and Zhou, Jian, additional

Published
2017
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22. Circumventing intratumoral heterogeneity to identify potential therapeutic targets in hepatocellular carcinoma

Author

Huang, Ao, primary, Zhao, Xin, additional, Yang, Xin-Rong, additional, Li, Fu-Qiang, additional, Zhou, Xin-Lan, additional, Wu, Kui, additional, Zhang, Xin, additional, Sun, Qi-Man, additional, Cao, Ya, additional, Zhu, Hong-Mei, additional, Wang, Xiang-Dong, additional, Yang, Huan-Ming, additional, Wang, Jian, additional, Tang, Zhao-You, additional, Hou, Yong, additional, Fan, Jia, additional, and Zhou, Jian, additional

Published
2017
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23. Naive Treg-like CCR7+ mononuclear cells indicate unfavorable prognosis in hepatocellular carcinoma

Author

Shi, Jie-Yi, primary, Duan, Meng, additional, Sun, Qi-Man, additional, Yang, Liuxiao, additional, Wang, Zhi-Chao, additional, Mynbaev, Ospan A., additional, He, Yi-Feng, additional, Wang, Ling-Yan, additional, Zhou, Jian, additional, Tang, Qi-Qun, additional, Cao, Ya, additional, Fan, Jia, additional, Wang, Xiao-Ying, additional, and Gao, Qiang, additional

Published
2016
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26. Plasma MicroRNA, a Potential Biomarker for Acute Rejection After Liver Transplantation

Author

Hu, Jie, primary, Wang, Zheng, additional, Tan, Chang-Jun, additional, Liao, Bo-Yi, additional, Zhang, Xin, additional, Xu, Min, additional, Dai, Zhi, additional, Qiu, Shuang-Jian, additional, Huang, Xiao-Wu, additional, Sun, Jian, additional, Sun, Qi-Man, additional, He, Yi-Feng, additional, Song, Kang, additional, Pan, Qi, additional, Wu, Ying, additional, Fan, Jia, additional, and Zhou, Jian, additional

Published
2013
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27. Genetic Variations in Plasma Circulating DNA of HBV-Related Hepatocellular Carcinoma Patients Predict Recurrence after Liver Transplantation

Author

Hu, Jie, primary, Wang, Zheng, additional, Fan, Jia, additional, Dai, Zhi, additional, He, Yi-Feng, additional, Qiu, Shuang-Jian, additional, Huang, Xiao-Wu, additional, Sun, Jian, additional, Xiao, Yong-Sheng, additional, Song, Kang, additional, Shi, Ying-Hong, additional, Sun, Qi-Man, additional, Yang, Xin-Rong, additional, Shi, Guo-Ming, additional, Yu, Lei, additional, Yang, Guo-Huan, additional, Ding, Zhen-Bin, additional, Gao, Qiang, additional, Tang, Zhao-You, additional, and Zhou, Jian, additional

Published
2011
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29. Macro CD5L + deteriorates CD8 + T cells exhaustion and impairs combination of Gemcitabine-Oxaliplatin-Lenvatinib-anti-PD1 therapy in intrahepatic cholangiocarcinoma.

Author

Lu JC, Wu LL, Sun YN, Huang XY, Gao C, Guo XJ, Zeng HY, Qu XD, Chen Y, Wu D, Pei YZ, Meng XL, Zheng YM, Liang C, Zhang PF, Cai JB, Ding ZB, Yang GH, Ren N, Huang C, Wang XY, Gao Q, Sun QM, Shi YH, Qiu SJ, Ke AW, Shi GM, Zhou J, Sun YD, and Fan J

Subjects
Humans, Oxaliplatin therapeutic use, Gemcitabine, CD8-Positive T-Lymphocytes, Bile Ducts, Intrahepatic, Apoptosis Regulatory Proteins, Receptors, Scavenger, Cholangiocarcinoma drug therapy, Cholangiocarcinoma genetics, Cholangiocarcinoma pathology, Bile Duct Neoplasms drug therapy, Bile Duct Neoplasms pathology, Phenylurea Compounds, Quinolines
Abstract

Intratumoral immune status influences tumor therapeutic response, but it remains largely unclear how the status determines therapies for patients with intrahepatic cholangiocarcinoma. Here, we examine the single-cell transcriptional and TCR profiles of 18 tumor tissues pre- and post- therapy of gemcitabine plus oxaliplatin, in combination with lenvatinib and anti-PD1 antibody for intrahepatic cholangiocarcinoma. We find that high CD8 GZMB + and CD8 proliferating proportions and a low Macro CD5L + proportion predict good response to the therapy. In patients with a poor response, the CD8 GZMB + and CD8 proliferating proportions are increased, but the CD8 GZMK + proportion is decreased after the therapy. Transition of CD8 proliferating and CD8 GZMB + to CD8 GZMK + facilitates good response to the therapy, while Macro CD5L + -CD8 GZMB + crosstalk impairs the response by increasing CTLA4 in CD8 GZMB + . Anti-CTLA4 antibody reverses resistance of the therapy in intrahepatic cholangiocarcinoma. Our data provide a resource for predicting response of the combination therapy and highlight the importance of CD8 + T-cell status conversion and exhaustion induced by Macro CD5L + in influencing the response, suggesting future avenues for cancer treatment optimization., (© 2024. The Author(s).)

Published
2024
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30. Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway.

Author

Fu XT, Dai Z, Song K, Zhang ZJ, Zhou ZJ, Zhou SL, Zhao YM, Xiao YS, Sun QM, Ding ZB, and Fan J

Subjects
Carcinoma, Hepatocellular pathology, Epithelial-Mesenchymal Transition genetics, Gene Expression Regulation, Neoplastic, Hep G2 Cells, Humans, Interleukin-8 genetics, Janus Kinase 2 genetics, Liver Neoplasms pathology, Macrophages metabolism, STAT3 Transcription Factor genetics, Signal Transduction genetics, Snail Family Transcription Factors, Transcription Factors genetics, Carcinoma, Hepatocellular genetics, Interleukin-8 metabolism, Janus Kinase 2 biosynthesis, Liver Neoplasms genetics, STAT3 Transcription Factor biosynthesis, Transcription Factors biosynthesis
Abstract

Macrophages are a major component of the leukocyte infiltrate of tumors and play a pivotal role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which macrophages promote HCC invasion are poorly understood. The present study was undertaken to investigate the relationship between macrophages and epithelial-mesenchymal transition (EMT) of HCC. Double-staining immunohistochemistry was used to observe the association between macrophages and EMT markers in clinical HCC samples and it showed that EMT primarily occurred at the edge of the tumor nest, in which infiltrating macrophages were always observed. This indicated that CD68 which is a marker of macrophages, was correlated with EMT marker levels. In addition, after being cultured with macrophages for 24 h, the ability of HCC cells to migrate and invade increased, Snail and N-Cadherin expression was upregulated, and E-Cadherin was downregulated. An antibody array assay was applied to analyze the supernatant of these cultures and it demonstrated IL-8 increased significantly in the macrophage co-culture system. Finally, the role of macrophage-derived IL-8 in the invasion of HCC cells was assayed, and downstream signaling pathways were also investigated. We found that IL-8: i) may induce EMT and promote HCC cell migration and invasion and ii) is associated with the JAK2/STAT3/Snail signaling pathway. Taking together, these findings revealed that macrophages that have infiltrated tumors may induce epithelial-mesenchymal transition of HCC cells via the IL-8 activated JAK2/STAT3/Snail pathway. Thus, this may offer a potential target for developing new HCC therapies.

Published
2015
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31. [Interferon-alpha upregulates thymidine phosphorylase expression via JAK-STAT transcriptional activation and mRNA stabilization in human hepatocellular carcinoma SMMC-7721 cells].

Author

Xiao YS, Zhou J, Fan J, Sun QM, Zhao Y, Sun RX, Liu YK, and Tang ZY

Subjects
Carcinoma, Hepatocellular pathology, Cell Line, Tumor, Dose-Response Relationship, Drug, Enzyme Inhibitors pharmacology, Gene Expression Regulation, Neoplastic, Humans, Interferon-alpha administration & dosage, Janus Kinases metabolism, Liver Neoplasms pathology, RNA, Messenger metabolism, STAT1 Transcription Factor metabolism, Thymidine Phosphorylase genetics, Transcriptional Activation drug effects, Tyrphostins pharmacology, Carcinoma, Hepatocellular enzymology, Interferon-alpha pharmacology, Liver Neoplasms enzymology, Thymidine Phosphorylase biosynthesis
Abstract

Objective: To examine how the thymidine phosphorylase (TP) gene expression is upregulated by interferon-alpha (IFN-alpha) in human hepatocellular carcinoma SMMC-7721 cells., Methods: TP mRNA levels were determined by RT-PCR. Whether the JAK-STAT cascade mediates IFN-alpha-induced TP mRNA expression was studied by pretreatment with Janus Kinase (JAK) inhibitor, AG-490. Effects of IFN-alpha on TP mRNA stability were detected with additional actinomycin D., Results: The expression of TP mRNA was induced by IFN-alpha in a dose- and time-dependent manner in SMMC-7721 (human hepatocellular carcinoma) cells. TP mRNA levels rose at 8 h, reached the peak value at 12 h, and remained at a high level up to 72 h in SMMC-7721 cells treated with IFN-alpha 10000 U/ml. IFN-alpha at a dose of 5000 or 10000 U/ml up-regulated TP expression about 3 fold compared with that of non-treated cells (P < 0.05). Induction of TP mRNA expression by IFN-alpha was significantly inhibited in SMMC-7721 cells by pretreatment with AG-490, in comparison with that treated with IFN-alpha alone. Pretreatment of SMMC-7721 cells with IFN-alpha 10000 U/ml for 24 h caused a substantial stabilization of TP mRNA, with a half-live of 35.8 h, compared with 8.5 hr in the control SMMC-7721 cells., Conclusion: IFN-alpha at certain doses upregulates TP mRNA expression via both JAK-STAT transcriptional activation and post-transcriptional mRNA stabilization in human hepatocellular carcinoma SMMC-7721 cells.

Published
2008

32. Capecitabine inhibits postoperative recurrence and metastasis after liver cancer resection in nude mice with relation to the expression of platelet-derived endothelial cell growth factor.

Author

Zhou J, Tang ZY, Fan J, Wu ZQ, Ji Y, Xiao YS, Shi YH, Li XM, Sun QM, Liu YK, and Ye SL

Subjects
Animals, Capecitabine, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular prevention & control, Fluorouracil analogs & derivatives, Humans, Liver Neoplasms, Experimental metabolism, Liver Neoplasms, Experimental prevention & control, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Metastasis drug therapy, Postoperative Care, Transplantation, Heterologous, Antimetabolites, Antineoplastic therapeutic use, Carcinoma, Hepatocellular surgery, Deoxycytidine analogs & derivatives, Deoxycytidine therapeutic use, Liver Neoplasms, Experimental surgery, Neoplasm Recurrence, Local drug therapy, Thymidine Phosphorylase metabolism
Abstract

Purpose: This study was to investigate the effect of capecitabine on recurrent tumor and metastasis after curative resection of liver cancer, xenograft of a highly metastatic human hepatocellular carcinoma (HCC) tumor (LCI-D20), with special reference to the expression of platelet-derived endothelial cell growth factor (PD-ECGF)., Experimental Design: LCI-D20 and LCI-D35 (a low metastatic human HCC model) liver tumors were orthotopically implanted in 96 nude mice and divided into a treatment group (24 LCI-D20 mice and 24 LCI-D35 mice) and a prevention group (48 LCI-D20 mice). In the prevention group, curative resection of liver tumors was done 10 days after the orthotopic implantation of LCI-D20 tumor. Arabic gum (control), 5-fluorouracil (5-FU), and capecitabine were administrated respectively to all of the 96 mice., Results: In the treatment group, tumor volume was 468 +/- 138, 442 +/- 81, and 240 +/- 119 mm3 (P<0.01) in the control, 5-FU, and capecitabine subgroups, respectively, in LCI-D20 mice, whereas it was 168 +/- 35, 164 +/- 23, and 144 +/- 21 mm3 (P>0.05), respectively, in LCI-D35 mice. In the prevention group, incidence of liver recurrence in the control, 5-FU, and capecitabine subgroups was 100, 100, and 50%; lung metastasis being 100, 100, and 17%; and life span being 31 +/- 5, 37 +/- 5, and 77 +/- 19 days, respectively. PD-ECGF was highly expressed in HCC and its metastatic tissues in LCI-D20 mice and hardly expressed in HCC tissues in LCI-D35 mice., Conclusions: Capecitabine inhibits tumor growth and metastatic recurrence after resection of HCC in highly metastatic nude mice model. The effect of capecitabine may be attributed to the high expression of PD-ECGF in tumors.

Published
2003

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