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5. Integrative analysis reveals different feature of intrahepatic cholangiocarcinoma subtypes.

Author

Chen, Zhuomiaoyu, Gao, Jie, Li, Zuyin, Ma, Delin, Wang, Yang, Cheng, Qian, Zhu, Jiye, and Li, Zhao

Subjects
GENE expression, RNA sequencing, OVERALL survival, PI3K/AKT pathway, SURVIVAL rate
Abstract

Background & Aims: Intrahepatic cholangiocarcinoma (iCCA) has two main histological subtypes: large and small duct‐type iCCA, which are characterized by different clinicopathological features. This study was conducted with the purpose of expanding our understanding of their differences in molecular features and immune microenvironment. Methods: We selected 132 patients who underwent radical surgery at our department between 2015 and 2021 for clinical and survival analyses. Whole‐exome sequencing was performed to analyse mutational landscapes. Bulk RNA sequencing and single‐cell RNA sequencing data were used for pathway enrichment and immune infiltration analyses based on differentially expressed genes. The function of PPP1R1B was analysed both in vitro and in vivo and the gene mechanism was further investigated. Results: We found that large duct‐type iCCA had worse overall survival and recurrence‐free survival rates than small duct‐type iCCA. Mutations in ARID1A, DOT1L and ELF3 usually occur in large duct‐type iCCA, whereas mutations in IDH1 and BAP1 occur in small duct‐type iCCA. Among the differentially expressed genes, we found that PPP1R1B was highly expressed in large duct‐type iCCA tumour tissues. Expression of PPP1R1B promoted cell proliferation, migration and invasion and indicated a worse prognosis. A combination of USF2 with the promoter of PPP1R1B can enhance gene expression in iCCA, which may further affect the expression of genes such as AHNAK, C4BPA and activating the PI3K/AKT pathway. Conclusions: Our findings extend our understanding of large and small duct‐type iCCA. In addition, PPP1R1B may serve as a potential marker and therapeutic target for large duct‐type iCCA. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Mechanistic Analysis of the Stress and Displacement Evolutions of Asphalt Mixtures Based on Finite Element Simulation.

Author

Liu, Dengao, Zhang, Haitao, Sun, Junfeng, Liu, Dongjie, and Zhu, Jiye

Subjects
STRAINS & stresses (Mechanics), STRESS concentration, MIXTURES
Abstract

To study the internal stress transfer law and the evolution of the fine structure of asphalt mixtures after being subjected to traffic load during the service phase, finite element (FE) models of porous asphalt mixtures (PAMs) and dense asphalt mixtures (DAMs) were developed for virtual uniaxial compression tests. By controlling the two asphalt mixtures to produce different longitudinal deformation, their damage patterns in the service phase are analyzed from a fine perspective. The results show that PAMs are capable of forming internal force chains when resisting external loads, and the displacement generated within the PAM is not uniformly distributed. Moreover, when resisting external loads, the internal stress distribution of DAMs is more uniform, as is the internal displacement distribution. The stress transfer law of the PAM is more conducive to transferring the load from the upper surface to the lower surface of the mixture than that of the DAM. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Supplementary Figure from Postoperative Plasmacytoid Dendritic Cells Secrete IFNα to Promote Recruitment of Myeloid-Derived Suppressor Cells and Drive Hepatocellular Carcinoma Recurrence

Author

Pang, Li, primary, Yeung, Oscar W.H., primary, Ng, Kevin T.P., primary, Liu, Hui, primary, Zhu, Jiye, primary, Liu, Jiang, primary, Yang, Xinxiang, primary, Ding, Tao, primary, Qiu, Wenqi, primary, Wang, Yuewen, primary, Chiu, T.L. Shirley, primary, Chen, Zhiwei, primary, Lo, Chung-Mau, primary, and Man, Kwan, primary

Published
2023
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15. Data from Postoperative Plasmacytoid Dendritic Cells Secrete IFNα to Promote Recruitment of Myeloid-Derived Suppressor Cells and Drive Hepatocellular Carcinoma Recurrence

Author

Pang, Li, primary, Yeung, Oscar W.H., primary, Ng, Kevin T.P., primary, Liu, Hui, primary, Zhu, Jiye, primary, Liu, Jiang, primary, Yang, Xinxiang, primary, Ding, Tao, primary, Qiu, Wenqi, primary, Wang, Yuewen, primary, Chiu, T.L. Shirley, primary, Chen, Zhiwei, primary, Lo, Chung-Mau, primary, and Man, Kwan, primary

Published
2023
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16. Supplementary Data from Postoperative Plasmacytoid Dendritic Cells Secrete IFNα to Promote Recruitment of Myeloid-Derived Suppressor Cells and Drive Hepatocellular Carcinoma Recurrence

Author

Pang, Li, primary, Yeung, Oscar W.H., primary, Ng, Kevin T.P., primary, Liu, Hui, primary, Zhu, Jiye, primary, Liu, Jiang, primary, Yang, Xinxiang, primary, Ding, Tao, primary, Qiu, Wenqi, primary, Wang, Yuewen, primary, Chiu, T.L. Shirley, primary, Chen, Zhiwei, primary, Lo, Chung-Mau, primary, and Man, Kwan, primary

Published
2023
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17. Guidelines for the Diagnosis and Treatment of Primary Liver Cancer (2022 Edition)

Author

Zhou, Jian, primary, Sun, Huichuan, additional, Wang, Zheng, additional, Cong, Wenming, additional, Zeng, Mengsu, additional, Zhou, Weiping, additional, Bie, Ping, additional, Liu, Lianxin, additional, Wen, Tianfu, additional, Kuang, Ming, additional, Han, Guohong, additional, Yan, ZhiPing, additional, Wang, Maoqiang, additional, Liu, Ruibao, additional, Lu, Ligong, additional, Ren, Zhenggang, additional, Zeng, ZhaoChong, additional, Liang, Ping, additional, Liang, Changhong, additional, Chen, Min, additional, Yan, Fuhua, additional, Wang, Wenping, additional, Hou, Jinlin, additional, Ji, Yuan, additional, Yun, Jingping, additional, Bai, Xueli, additional, Cai, Dingfang, additional, Chen, Weixia, additional, Chen, Yongjun, additional, Cheng, Wenwu, additional, Cheng, Shuqun, additional, Dai, Chaoliu, additional, Guo, Wenzhi, additional, Guo, Yabing, additional, Hua, Baojin, additional, Huang, Xiaowu, additional, Jia, Weidong, additional, Li, Qiu, additional, Li, Tao, additional, Li, Xun, additional, Li, Yaming, additional, Li, Yexiong, additional, Liang, Jun, additional, Ling, Changquan, additional, Liu, Tianshu, additional, Liu, Xiufeng, additional, Lu, Shichun, additional, Lv, Guoyue, additional, Mao, Yilei, additional, Meng, Zhiqiang, additional, Peng, Tao, additional, Ren, Weixin, additional, Shi, Hongcheng, additional, Shi, Guoming, additional, Shi, Ming, additional, Song, Tianqiang, additional, Tao, Kaishan, additional, Wang, Jianhua, additional, Wang, Kui, additional, Wang, Lu, additional, Wang, Wentao, additional, Wang, Xiaoying, additional, Wang, Zhiming, additional, Xiang, Bangde, additional, Xing, Baocai, additional, Xu, Jianming, additional, Yang, Jiamei, additional, Yang, Jianyong, additional, Yang, Yefa, additional, Yang, Yunke, additional, Ye, Shenglong, additional, Yin, Zhenyu, additional, Zeng, Yong, additional, Zhang, Bixiang, additional, Zhang, Boheng, additional, Zhang, Leida, additional, Zhang, Shuijun, additional, Zhang, Ti, additional, Zhang, Yanqiao, additional, Zhao, Ming, additional, Zhao, Yongfu, additional, Zheng, Honggang, additional, Zhou, Ledu, additional, Zhu, Jiye, additional, Zhu, Kangshun, additional, Liu, Rong, additional, Shi, Yinghong, additional, Xiao, Yongsheng, additional, Zhang, Lan, additional, Yang, Chun, additional, Wu, Zhifeng, additional, Dai, Zhi, additional, Chen, Minshan, additional, Cai, Jianqiang, additional, Wang, Weilin, additional, Cai, Xiujun, additional, Li, Qiang, additional, Shen, Feng, additional, Qin, Shukui, additional, Teng, Gaojun, additional, Dong, Jiahong, additional, and Fan, Jia, additional

Published
2023
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22. Isoformic PD-1-mediated immunosuppression underlies resistance to PD-1 blockade in hepatocellular carcinoma patients

Author

Tan, Zhiwu, primary, Chiu, Mei Sum, additional, Yang, Xinxiang, additional, Yue, Ming, additional, Cheung, Tan To, additional, Zhou, Dongyan, additional, Wang, Yuewen, additional, Chan, Anthony Wing-Hung, additional, Yan, Chi Wing, additional, Kwan, Ka Yi, additional, Wong, Yik Chun, additional, Li, Xin, additional, Zhou, Jingying, additional, To, Ka Fai, additional, Zhu, Jiye, additional, Lo, Chung Mau, additional, Cheng, Alfred Sze-Lok, additional, Chan, Stephen Lam, additional, Liu, Li, additional, Song, You-Qiang, additional, Man, Kwan, additional, and Chen, Zhiwei, additional

Published
2022
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23. Postoperative Plasmacytoid Dendritic Cells Secrete IFNα to Promote Recruitment of Myeloid-Derived Suppressor Cells and Drive Hepatocellular Carcinoma Recurrence

Author

Pang, Li, primary, Yeung, Oscar W.H., additional, Ng, Kevin T.P., additional, Liu, Hui, additional, Zhu, Jiye, additional, Liu, Jiang, additional, Yang, Xinxiang, additional, Ding, Tao, additional, Qiu, Wenqi, additional, Wang, Yuewen, additional, Chiu, T.L. Shirley, additional, Chen, Zhiwei, additional, Lo, Chung-Mau, additional, and Man, Kwan, additional

Published
2022
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30. Cyclooxygenase-2 expressed hepatocellular carcinoma induces cytotoxic T lymphocytes exhaustion through M2 macrophage polarization

Author

Xun, Xiaodong, Zhang, Changkun, Wang, Siqi, Hu, Shihua, Xiang, Xiao, Cheng, Qian, Li, Zhao, Wang, Yang, and Zhu, Jiye

Subjects
Original Article
Abstract

Objective: Due to the tumor immune microenvironment (TIME) complexity and cancer heterogeneity, the clinical outcomes of hepatocellular carcinoma (HCC) are barely elicited from the conventional treatment options, even from the promising anti-cancer immunotherapy. As a suppressive TIME-related marker, the role played by cyclooxygenase-2 (COX-2) in HCC TIME, and its potential effects on anti-cancer T cell immune response remains unknown. In our study, to investigate the COX-2-dependent immune regulation pathway, we verified that the macrophages phenotypes were correlated to COX-2/PGE2 expressions among HCC patients. A multi-cellular co-culture platform containing HCC cells, macrophages, and T cells were established to mimic HCC TIME in vitro and in animal model. M2 macrophage polarization and activated CD8(+) T cells exhaustion were observed under high COX-2 levels in HCC cells, with further evaluation using CRISPR/Cas9-based PTGS2 knocking out and COX-2 blockade (celecoxib) treatment controls. PGE2, TGF-β, Granzyme B, and IFN-γ levels were testified by flow cytometry and ELISA to fully understand the mechanism of COX-2 suppressive effects on T cell-based anti-HCC responses. The activation of the TGF-β pathway evaluated by auto-western blot in T cells was confirmed which increased the level of phosphorylated Smad3, phosphorylated Samd2, and FoxP1, leading to T cell de-lymphotoxin. In conclusion, high COX-2-expressing HCC cell lines can induce anti-tumor abilities exhaustion in activated CD8(+) T cell through M2 TAMs polarization and TGF beta pathway. COX-2 inhibitors may reduce the inhibitory effect on CD8(+) T cells through regulating TAMs in TIME, thus enhance the T cell-based cytotoxicity and improve the prognosis of HCC patients.

Published
2021

32. IDH Mutation Subgroup Status Associates with Intratumor Heterogeneity and the Tumor Microenvironment in Intrahepatic Cholangiocarcinoma

Author

Xiang, Xiao, primary, Liu, Ziyang, additional, Zhang, Chong, additional, Li, Zhao, additional, Gao, Jie, additional, Zhang, Changkun, additional, Cao, Qi, additional, Cheng, Jinghui, additional, Liu, Hengkang, additional, Chen, Dingbao, additional, Cheng, Qian, additional, Zhang, Ning, additional, Xue, Ruidong, additional, Bai, Fan, additional, and Zhu, Jiye, additional

Published
2021
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33. Isoformic PD-1-mediated immunosuppression underlies resistance to PD-1 blockade in hepatocellular carcinoma patients

Author

Tan, Zhiwu, Chiu, Mei Sum, Yang, Xinxiang, Yue, Ming, Cheung, Tan To, Zhou, Dongyan, Wang, Yuewen, Chan, Anthony Wing-Hung, Yan, Chi Wing, Kwan, Ka Yi, Wong, Yik Chun, Li, Xin, Zhou, Jingying, To, Ka Fai, Zhu, Jiye, Lo, Chung Mau, Cheng, Alfred Sze-Lok, Chan, Stephen Lam, Liu, Li, Song, You-Qiang, Man, Kwan, and Chen, Zhiwei

Abstract

ObjectiveImmune checkpoint blockade (ICB) has improved cancer treatment, yet why most hepatocellular carcinoma (HCC) patients are resistant to PD-1 ICB remains elusive. Here, we elucidated the role of a programmed cell death protein 1 (PD-1) isoform, Δ42PD-1, in HCC progression and resistance to nivolumab ICB.DesignWe investigated 74 HCC patients in three cohorts, including 41 untreated, 28 treated with nivolumab and 5 treated with pembrolizumab. Peripheral blood mononuclear cells from blood samples and tumour infiltrating lymphocytes from tumour tissues were isolated for immunophenotyping. The functional significance of Δ42PD-1 was explored by single-cell RNA sequencing analysis and validated by functional and mechanistic studies. The immunotherapeutic efficacy of Δ42PD-1 monoclonal antibody was determined in HCC humanised mouse models.ResultsWe found distinct T cell subsets, which did not express PD-1 but expressed its isoform Δ42PD-1, accounting for up to 71% of cytotoxic T lymphocytes in untreated HCC patients. Δ42PD-1+T cells were tumour-infiltrating and correlated positively with HCC severity. Moreover, they were more exhausted than PD-1+T cells by single T cell and functional analysis. HCC patients treated with anti-PD-1 ICB showed effective PD-1 blockade but increased frequencies of Δ42PD-1+T cells over time especially in patients with progressive disease. Tumour-infiltrated Δ42PD-1+T cells likely sustained HCC through toll-like receptors-4-signalling for tumourigenesis. Anti-Δ42PD-1 antibody, but not nivolumab, inhibited tumour growth in three murine HCC models.ConclusionOur findings not only revealed a mechanism underlying resistance to PD-1 ICB but also identified anti-Δ42PD-1 antibody for HCC immunotherapy.

Published
2023
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36. Guidelines for the Diagnosis and Treatment of Hepatocellular Carcinoma (2019 Edition)

Author

Zhou, Jian, primary, Sun, Huichuan, additional, Wang, Zheng, additional, Cong, Wenming, additional, Wang, Jianhua, additional, Zeng, Mengsu, additional, Zhou, Weiping, additional, Bie, Ping, additional, Liu, Lianxin, additional, Wen, Tianfu, additional, Han, Guohong, additional, Wang, Maoqiang, additional, Liu, Ruibao, additional, Lu, Ligong, additional, Ren, Zhengang, additional, Chen, Minshan, additional, Zeng, Zhaochong, additional, Liang, Ping, additional, Liang, Changhong, additional, Chen, Min, additional, Yan, Fuhua, additional, Wang, Wenping, additional, Ji, Yuan, additional, Yun, Jingping, additional, Cai, Dingfang, additional, Chen, Yongjun, additional, Cheng, Wenwu, additional, Cheng, Shuqun, additional, Dai, Chaoliu, additional, Guo, Wenzhi, additional, Hua, Baojin, additional, Huang, Xiaowu, additional, Jia, Weidong, additional, Li, Yaming, additional, Li, Yexiong, additional, Liang, Jun, additional, Liu, Tianshu, additional, Lv, Guoyue, additional, Mao, Yilei, additional, Peng, Tao, additional, Ren, Weixin, additional, Shi, Hongcheng, additional, Shi, Guoming, additional, Tao, Kaishan, additional, Wang, Wentao, additional, Wang, Xiaoying, additional, Wang, Zhiming, additional, Xiang, Bangde, additional, Xing, Baocai, additional, Xu, Jianming, additional, Yang, Jiamei, additional, Yang, Jianyong, additional, Yang, Yefa, additional, Yang, Yunke, additional, Ye, Shenglong, additional, Yin, Zhengyu, additional, Zhang, Bixiang, additional, Zhang, Boheng, additional, Zhang, Leida, additional, Zhang, Shuijun, additional, Zhang, Ti, additional, Zhao, Yongfu, additional, Zheng, Honggang, additional, Zhu, Jiye, additional, Zhu, Kangshun, additional, Liu, Rong, additional, Shi, Yinghong, additional, Xiao, Yongsheng, additional, Dai, Zhi, additional, Teng, Gaojun, additional, Cai, Jianqiang, additional, Wang, Weilin, additional, Cai, Xiujun, additional, Li, Qiang, additional, Shen, Feng, additional, Qin, Shukui, additional, Dong, Jiahong, additional, and Fan, Jia, additional

Published
2020
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38. Noncoding RNAs Act as Tumor-Derived Molecular Components in Inducing Premetastatic Niche Formation

Author

Zhang, Zhedong, Qiao, Jiao, Zhang, Dafang, Zhu, Weihua, Zhu, Jiye, Leng, Xisheng, and Li, Shu

Subjects
Article Subject
Abstract

Cancer metastasis has been demonstrated as it is the culmination of a cascade of priming steps. Increasing evidence has shown that tumor-derived molecular components (TDMCs) are known as extra cellular vesicle and nonvesicle factors and serve as versatile intercellular communication vehicles which can mediate signaling in the tumor microenvironment while creating the premetastatic niche. Noncoding RNAs (ncRNAs) as one of the TDMCs have been proved in participating in the formation of the premetastatic niche. Understanding the premetastatic niche formation mechanisms through TDMCs, especially ncRNAs may open a new avenue for cancer metastasis therapeutic strategies. In this review, recent findings regarding ncRNAs function were summarized, and then the interaction with the premetastatic niche formation was studied, which highlight the potential of using ncRNAs for cancer diagnosis and therapeutic effect.

Published
2019
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43. TIGIT Can Exert Immunosuppressive Effects on CD8+T Cells by the CD155/TIGIT Signaling Pathway for Hepatocellular Carcinoma In Vitro

Author

Zhang, Changkun, Wang, Yang, Xun, Xiaodong, Wang, Siqi, Xiang, Xiao, Hu, Shihua, Cheng, Qian, Guo, Jinghang, Li, Zhao, and Zhu, Jiye

Abstract

Supplemental Digital Content is available in the text.The efficacy of adoptive cellular immunotherapy against cancer cells is limited due to the presence of immunosuppressive cells within the solid tumor microenvironment. The upregulation of certain coinhibitory receptors may lead to exhaustion of the immune effector cells. T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) is an immune inhibitory receptor expressed by regulatory T cells and activated T cells and natural killer cells. The aim of this study was to determine the immunosuppressive effects of CD155/TIGIT signaling on CD8+T cells of adoptive cellular immunotherapy in hepatocellular carcinoma (HCC). Our studies found that CD155 was overexpressed in HCC, and CD155hiHCC cells upregulated TIGIT on CD8+T cells, which decreased the secretion of interferon-γ, tumor necrosis factor-α, and interleukin-17A and increased that of interleukin-10 from the effector cells. However, TIGIT blockade or CD155-knockdown reversed the inhibitory effect of HCC cells on CD8+T-cell effector function. These results indicate that TIGIT can exert an immunosuppressive effect on CD8 T cells by modulating cytokine production through CD155, and is a promising target to optimize adoptive cellular immunotherapy against HCC.

Published
2020
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49. Effects of harmaline on cell growth of human liver cancer through the p53/p21 and Fas/FasL signaling pathways.

Author

Xu, Bin, Li, Minpeng, Yu, Yuan, He, Jun, Hu, Siqin, Pan, Meng, Lu, Shifeng, Liao, Ke, Pan, Zhuang, Zhou, Yanxun, and Zhu, Jiye

Subjects
LIVER cancer, ENZYME-linked immunosorbent assay, CANCER cell proliferation, CANCER cell growth, FLOW cytometry, TUMOR necrosis factor receptors
Abstract

The effects of harmaline on the viability and apoptosis of human liver carcinoma were investigated in vitro. HepG2 cells were treated with harmaline (0-10 μM), and the proliferation and apoptosis of HepG2 cells were investigated using an MTT assay and flow cytometry, respectively. The protein expression of cellular tumor antigen p53 (p53), cyclin-dependent kinase inhibitor 1 (p21), tumor necrosis factor receptor superfamily member 6 (Fas), Fas ligand (FasL) and caspase-8 was subsequently measured using western blotting. In addition, an ELISA was used to analyze caspase-8/3 activity. Harmaline significantly increased p53, p21, Fas and FasL protein expression in HepG2 cells. Additionally, treatment with harmaline significantly increased the expression of caspase-8 and caspase-8/3 activity. The results from the present study suggest that harmaline suppresses the viability, but induces the apoptosis, of human liver carcinoma cells through upregulation of the p53/p21 and Fas/FasL signaling pathways. [ABSTRACT FROM AUTHOR]

Published
2018
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