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139 results on '"Wu, Jindao"'

17. Retracted: M2 Macrophage–Derived Exosomes Facilitate HCC Metastasis by Transferring αMβ2 Integrin to Tumor Cells

Author

Wu, Jindao, primary, Gao, Wen, additional, Tang, Qiyun, additional, Yu, Yue, additional, You, Wei, additional, Wu, Zhengshan, additional, Fan, Ye, additional, Zhang, Long, additional, Wu, Chen, additional, Han, Guoyong, additional, Zuo, Xueliang, additional, Zhang, Yao, additional, Chen, Zhiqiang, additional, Ding, Wenzhou, additional, Li, Xiangcheng, additional, Lin, Fengming, additional, Shen, Hongbing, additional, Tang, Jinhai, additional, Zhang, Yaqin, additional, and Wang, Xuehao, additional

Published
2021
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21. Downregulated miR-621 promotes cell proliferation via targeting CAPRIN1 in hepatocellular carcinoma

Author

Zhang, Yao, You, Wei, Zhou, Haoming, Chen, Zhiqiang, Han, Guoyong, Zuo, Xueliang, Zhang, Long, Wu, Jindao, and Wang, Xuehao

Subjects
Original Article
Abstract

MicroRNAs (miRNAs) have been reported to play an essential role in tumor development and progression. However, the function of miR-621 in hepatocellular carcinoma (HCC) remains largely unexplored. In this study, we found that miR-621 was downregulated in the HCC specimens and cell lines, and lower expression of miR-621 indicated poor survival. Overexpression of miR-621 was shown to induce G0/G1 cell cycle arrest and inhibit cell proliferation in vitro and in vivo. Luciferase assays revealed that cell cycle-associated protein 1 (CAPRIN1) is a novel functional downstream target of miR-621. miR-621 could regulate c-MYC and cyclin D2 expression by directly targeting CAPRIN1. Further study revealed that CAPRIN1 was upregulated in the HCC specimens and cell lines. Restoration of CAPRIN1 neutralized the miR-621-induced cell cycle arrest and cell proliferation inhibition. Taken together, our findings suggest that miR-621 acts as a tumor suppressor gene in HCC progression by downregulating CAPRIN1 expression and could be a novel potential diagnostic and prognostic biomarker for HCC.

Published
2018

23. 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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24. 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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41. circLARP4 induces cellular senescence through regulating miR‐761/RUNX3/p53/p21 signaling in hepatocellular carcinoma.

Author

Chen, Zhiqiang, Zuo, Xueliang, Pu, Liyong, Zhang, Yao, Han, Guoyong, Zhang, Long, Wu, Jindao, and Wang, Xuehao

Abstract

Circular RNAs (circRNAs), a novel class of non‐coding RNAs, have emerged as indispensable modulators in human malignancies. Aberrant cellular senescence is a phenotype observed in various cancers. The association of circRNAs with cellular senescence in tumors is yet to determined. Here, we investigated the role of circLARP4 in cellular senescence and cell proliferation in hepatocellular carcinoma (HCC). Downregulated circLARP4 level was observed in HCC tissues and cell lines. Low expression level of circLARP4 independently predicted poor survival outcome. Gain‐of‐function and loss‐of‐function assays demonstrated that circLARP4 suppressed HCC cell proliferation, mediated cell cycle arrest and induced senescence in vitro. Levels of p53 and p21, 2 key regulatory molecules in cellular senescence, were increased in circLARP4‐overexpressed HCC cells and decreased in circLARP4‐silenced HCC cells. In vivo experiments further confirmed the tumor‐suppressing activity of circLARP4. Further mechanistic studies showed that circLARP4 dampened HCC progression by sponging miR‐761, thereby promoting the expression level of RUNX3 and activating the downstream p53/p21 signaling. Our study revealed the role of circLARP4/miR‐761/RUNX3/p53/p21 signaling in HCC progression, providing a potential survival predictor and therapeutic candidate for HCC. circLARP4 is downregulated in hepatocellular carcinoma. circLARP4 suppresses hepatocellular carcinoma cell proliferation, mediates cell cycle arrest and induces senescence. circLARP4 dampens hepatocellular carcinoma progression by sponging miR‐761, thereby promoting the expression of RUNX3 and activating the downstream p53/p21 signaling. [ABSTRACT FROM AUTHOR]

Published
2019
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43. Application of microwave ablation in the emergent control of intraoperative life-threatening tumor hemorrhage during hepatic surgeries.

Author

Zhou, Haoming, Wu, Jindao, Ling, Wei, Zhu, Deming, Lu, Ling, Wang, Xuehao, Pu, Liyong, and Kong, Lianbao

Subjects
*ABLATION techniques, *HEMORRHAGE treatment, *TREATMENT effectiveness, *LIVER surgery, PREVENTION of surgical complications
Abstract

Purpose: This study was designed to evaluate the efficacy and safety of microwave ablation (MWA) in the treatment of intraoperative life-threatening tumour haemorrhage during hepatic surgeries. Methods: Three cases of MWA application in the emergent control of life-threatening hepatic tumour haemorrhage were analysed and reported. Results: Satisfactory hemostasis for hepatic tumour rupture was achieved by MWA in all three cases. No major complications, such as post-operative haemorrhage, bile duct injury, liver abscess, colon perforation, skin burns, tumour seeding or renal dysfunction, were identified. Conclusions: MWA may be a feasible, effective and simple strategy for the emergent control of intraoperative hepatic tumour bleeding. To the best of our knowledge, this study represents the first reported cases of this novel application of MWA. [ABSTRACT FROM AUTHOR]

Published
2018
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44. Comparative Profiling of Triple-Negative Breast Carcinomas Tissue Glycoproteome by Sequential Purification of Glycoproteins and Stable Isotope Labeling

Author

Chen, Xiang, primary, Wu, Jindao, additional, Huang, Huaxing, additional, Ding, Qiang, additional, Liu, Xiaoan, additional, Chen, Lin, additional, Zha, Xiaoming, additional, Liang, Mengdi, additional, He, Jing, additional, Zhu, Qiannan, additional, Wang, Shui, additional, and Xia, Tiansong, additional

Published
2016
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49. Role of tumor-associated macrophages in hepatocellular carcinoma: impact, mechanism, and therapy.

Author

Zhang Y, Han G, Gu J, Chen Z, and Wu J

Subjects
Humans, Animals, Immunotherapy methods, Signal Transduction, Carcinoma, Hepatocellular immunology, Carcinoma, Hepatocellular therapy, Carcinoma, Hepatocellular pathology, Liver Neoplasms immunology, Liver Neoplasms therapy, Liver Neoplasms pathology, Tumor-Associated Macrophages immunology, Tumor-Associated Macrophages metabolism, Tumor Microenvironment immunology
Abstract

Hepatocellular carcinoma (HCC) is a highly frequent malignancy worldwide. The occurrence and progression of HCC is a complex process closely related to the polarization of tumor-associated macrophages (TAMs) in the tumor microenvironment (TME). The polarization of TAMs is affected by a variety of signaling pathways and surrounding cells. Evidence has shown that TAMs play a crucial role in HCC, through its interaction with other immune cells in the TME. This review summarizes the origin and phenotypic polarization of TAMs, their potential impacts on HCC, and their mechanisms and potential targets for HCC immunotherapy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhang, Han, Gu, Chen and Wu.)

Published
2024
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50. E2F1-mediated GINS2 transcriptional activation promotes tumor progression through PI3K/AKT/mTOR pathway in hepatocellular carcinoma.

Author

Zhang Y, Hao X, Han G, Lu Y, Chen Z, Zhang L, Wu J, and Wang X

Abstract

Hepatocellular carcinoma (HCC) has high morbidity and mortality rates. It is therefore imperative to study the underlying mechanism of HCC to identify potential prognostic biomarkers and therapeutic targets. Recently, GINS2 has been identified to be a cancer-promoting gene in different cancer types. Nevertheless, the exact mechanism of GINS2 in HCC remains to be elucidated. To systematically explore the significance of GINS2, we first assessed the relative expression of GINS2 in pan-cancers based on data obtained from the HCCDB, TIMER, and TCGA databases. Then, we explored the clinical significance of GINS2 in HCC through Kaplan-Meier method as well as univariate and multivariate cox regression analysis. Additionally, functional enrichment analysis of GINS2 was done through GO, KEGG, PPI network, and immune cell infiltration analyses. Functional experiments were also conducted to investigate the biological significance of GINS2 in HCC cell lines. Our research revealed that GINS2 is involved in HCC progression and highlighted its potential value as a crucial diagnostic and therapeutic target for HCC., Competing Interests: None., (AJCR Copyright © 2022.)

Published
2022

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