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529 results on '"Liang, Huifang"'

52. SRSF10 inhibition prevents HCC growth and metastasis and enhances the anti-PD-L1- mediated tumor suppression

Author

Luo, Xiangyuan, primary, Zhang, Zerui, additional, Wang, Yijun, additional, Sun, Mengyu, additional, Hu, Dian, additional, Jiang, Junqing, additional, Wang, Yufei, additional, Ji, Xiaoyu, additional, Chen, Xiaoping, additional, Zhang, Bixiang, additional, Liang, Huifang, additional, Li, Yiwei, additional, Liu, Bifeng, additional, Nie, Yongzhan, additional, Wu, Kaichun, additional, Fan, Daiming, additional, Liu, Danfei, additional, Huang, Wenjie, additional, and Xia, Limin, additional

Published
2023
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56. Bone Lesion‐Derived Extracellular Vesicles Fuel Prometastatic Cascades in Hepatocellular Carcinoma by Transferring ALKBH5‐Targeting miR‐3190‐5p

Author

Han, Shenqi, primary, Xue, Lin, additional, Wei, Yi, additional, Yong, Tuying, additional, Jia, Wenlong, additional, Qi, Yongqiang, additional, Luo, Yiming, additional, Liang, Junnan, additional, Wen, Jingyuan, additional, Bie, Nana, additional, Liang, Huifang, additional, Liu, Qiumeng, additional, Ding, Zeyang, additional, Yang, Xiangliang, additional, Gan, Lu, additional, Huang, Zhao, additional, Chen, Xiaoping, additional, and Zhang, Bixiang, additional

Published
2023
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59. Disrupting CCDC137-mediated LZTS2 and β-TrCP interaction in the nucleus inhibits hepatocellular carcinoma development via β-catenin and AKT

Author

Xu, Lei, Liu, Qiumeng, Liu, Hailing, Fan, Feimu, Li, Pengcheng, Yue, Shiwei, Mo, Jie, Liu, Zhicheng, Dong, Renshun, Zhang, Xuewu, Dong, Hanhua, Liang, Huifang, Chen, Xiaoping, Zhang, Bixiang, Chen, Lin, and Chen, Jin

Abstract

Hepatocellular carcinoma (HCC) is a highly heterogeneous solid tumor, with its biological characteristics intricately linked to the activation of oncogenes. This research specifically explored CCDC137, a molecule within the CCDC family exhibiting the closest association with HCC. Our investigation aimed to unravel the role, underlying mechanisms, and potential therapeutic implications of CCDC137 in the context of HCC. We observed a close correlation between elevated CCDC137 expression and poor prognosis in HCC patients, along with a promotive effect on HCC progression in vitro and in vivo. Mechanistically, we identified LZTS2, a negative regulator of β-catenin, as the binding protein of CCDC137. CCDC137 facilitated K48-linked poly-ubiquitination of LZTS2 at lysine 467 via recruiting E3 ubiquitin ligase β-TrCP in the nucleus, triggering AKT phosphorylation and activation of β-catenin pathway. Moreover, the 1-75 domain of CCDC137 was responsible for the formation of the CCDC137-LZTS2-β-TrCP complex. Subsequently, designed peptides targeting the 1-75 domain of CCDC137 to disrupt CCDC137-LZTS2 interaction demonstrated efficacy in inhibiting HCC progression. This promising outcome was further supported by HCC organoids and patient-derived xenograft (PDX) models, underscoring the potential clinical utility of the peptides. This study elucidated the mechanism of the CCDC137-LZTS2-β-TrCP protein complex in HCC and offered clinically significant therapeutic strategies targeting this complex.

Published
2024
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60. Targeting MMP9 in CTNNB1 mutant hepatocellular carcinoma restores CD8+T cell-mediated antitumour immunity and improves anti-PD-1 efficacy

Author

Cai, Ning, Cheng, Kun, Ma, Yue, Liu, Sha, Tao, Ran, Li, Yani, Li, Danfeng, Guo, Bin, Jia, Wenlong, Liang, Huifang, Zhao, Jianping, Xia, Limin, Ding, Ze-yang, Chen, Jinhong, and Zhang, Wanguang

Abstract

ObjectiveThe gain of function (GOF) CTNNB1 mutations (CTNNB1GOF) in hepatocellular carcinoma (HCC) cause significant immune escape and resistance to anti-PD-1. Here, we aimed to investigate the mechanism of CTNNB1GOFHCC-mediated immune escape and raise a new therapeutic strategy to enhance anti-PD-1 efficacy in HCC.DesignRNA sequencing was performed to identify the key downstream genes of CTNNB1GOFassociated with immune escape. An in vitro coculture system, murine subcutaneous or orthotopic models, spontaneously tumourigenic models in conditional gene-knock-out mice and flow cytometry were used to explore the biological function of matrix metallopeptidase 9 (MMP9) in tumour progression and immune escape. Single-cell RNA sequencing and proteomics were used to gain insight into the underlying mechanisms of MMP9.ResultsMMP9 was significantly upregulated in CTNNB1GOFHCC. MMP9 suppressed infiltration and cytotoxicity of CD8+T cells, which was critical for CTNNB1GOFto drive the suppressive tumour immune microenvironment (TIME) and anti-PD-1 resistance. Mechanistically, CTNNB1GOFdownregulated sirtuin 2 (SIRT2), resulting in promotion of β-catenin/lysine demethylase 4D (KDM4D) complex formation that fostered the transcriptional activation of MMP9. The secretion of MMP9 from HCC mediated slingshot protein phosphatase 1 (SSH1) shedding from CD8+T cells, leading to the inhibition of C-X-C motif chemokine receptor 3 (CXCR3)-mediated intracellular of G protein-coupled receptors signalling. Additionally, MMP9 blockade remodelled the TIME and potentiated the sensitivity of anti-PD-1 therapy in HCC.ConclusionsCTNNB1GOFinduces a suppressive TIME by activating secretion of MMP9. Targeting MMP9 reshapes TIME and potentiates anti-PD-1 efficacy in CTNNB1GOFHCC.

Published
2024
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64. Targeting VPS72 inhibits ACTL6A/MYC axis activity in hepatocellular carcinoma progression

Author

Liu, Furong, primary, Liao, Zhibin, additional, Qin, Lu, additional, Zhang, Ze, additional, Zhang, Qiaofeng, additional, Han, Shenqi, additional, Zeng, Weifeng, additional, Zhang, Hongwei, additional, Liu, Yachong, additional, Song, Jia, additional, Chen, Wei, additional, Zhu, He, additional, Liang, Huifang, additional, Chen, Xiaoping, additional, Zhang, Bixiang, additional, and Zhang, Zhanguo, additional

Published
2023
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74. Ring finger protein 12 activates AKT signalling to promote the progression of liver cancer by interacting with EGFR.

Author

Yu, Chengpeng, Rao, Dean, Wang, Tiantian, Sheng, Jiaqi, Lv, Enjun, Zhang, Long, Lu, Xun, Yu, Jingjing, Liang, Huifang, Song, Jia, and Huang, Wenjie

Subjects
LIVER cancer, LIVER cells, EPIDERMAL growth factor receptors, CANCER cell proliferation, CANCER cell migration, CANCER invasiveness
Abstract

Liver cancer is one of the most common solid tumours, and ranks as the third leading cause of cancer‐associated mortality around the world. This study has linked RNF12 to the pathogenesis of liver cancer. Based on the analysis of patient samples and database data, high RNF12 expression was found in liver cancer, in correlation with worse clinicopathological features and a poor prognosis. Meantime, RNF12 could promote the progression of liver cancer in vitro and in vivo. Mechanistically, RNF12 could interact with EGFR and decrease the internalization of EGFR to activate EGF/EGFR signalling. In addition, PI3K‐AKT signalling takes part in the regulation of liver cancer cell proliferation and migration of RNF12. And AKT inhibitor MK2206 could reverse RNF12‐mediated cellular proliferation and migration in liver cancer. The possibility of the physical interaction between RNF12 and EGFR might lay a foundation to develop intervention strategies for liver cancer prevention and therapy. [ABSTRACT FROM AUTHOR]

Published
2023
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78. Observational data from the adalimumab post‐marketing PYRAMID registry of patients with Crohn's disease who became pregnant: A post hoc analysis

Author

Hart, Ailsa, primary, D’Haens, Geert, additional, Bereswill, Mareike, additional, Finney‐Hayward, Tricia, additional, Kalabic, Jasmina, additional, Levy, Gweneth, additional, Liang, Huifang, additional, Seow, Cynthia H., additional, Loftus, Edward V., additional, Panaccione, Remo, additional, Reinisch, Walter, additional, and Satsangi, Jack, additional

Published
2022
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80. LINC01608 activated by YY1 facilitate hepatocellular carcinoma progression by modulating the EGFR/ERK axis.

Author

Han, Mengzhen, Liu, Furong, Li, Xinxin, Zhang, Hongwei, Pan, Yonglong, Liu, Yachong, Zhu, He, Liang, Huifang, Chen, Xiaoping, Liao, Zhibin, Zhang, Zhanguo, and Zhang, Bixiang

Subjects
HEPATOCELLULAR carcinoma, EPIDERMAL growth factor receptors, LINCRNA, FLUORESCENCE in situ hybridization, IN situ hybridization
Abstract

Background: Long non‐coding RNAs (LncRNAs) have been demonstrated to associate with a variety of cancers. However, the mechanisms of LncRNAs in hepatocellular carcinoma (HCC) progression are still not fully clarified. Methods: LINC01608 expression level in HCC and adjacent normal tissues was detected by real‐time‐quantitively PCR (RT‐qPCR) in clinical samples and in situ hybridization (ISH) in tissue microarray. Several functional assays were performed to determine the biological effects of LINC01608 in HCC cells in vitro, while subcutaneous xenograft models and lung metastasis models in nude mice and immunohistochemistry (IHC) results showed the role of LINC01608 in HCC progression in vivo. The combination of LINC01608 with miR‐875‐5p and target genes was elucidated by dual‐luciferase report assays, RNA immunoprecipitation (RIP) assays and fluorescence in situ hybridization (FISH) assays. Finally, bioinformatics analysis and chromatin immunoprecipitation (CHIP) were performed to investigate the mechanism of Yin Yang‐1 (YY1) regulating LINC01608 transcription. Results: LINC01608 was overexpressed in HCC tissues, and high LINC01608 expression predicted poor overall survival (OS) and disease‐free survival (DFS) in HCC patients. LINC01608 could promote HCC cell proliferation, migration, invasion and epithelial‐mesenchymal transition (EMT) in vitro and in vivo. Furthermore, we demonstrated that LINC01608 could sponge to miR‐875‐5p and activate the EGFR/ERK pathway. Moreover, we identified transcriptional factor YY1 could bind to the promoter of LINC01608 and induce its transcription. Conclusion: LINC01608 could serve as a promising prognostic biomarker of HCC. YY1‐activated LINC01608 could promote HCC progression by associating with miR‐875‐5p to induce the EGFR/ERK signalling pathway. This discovery might provide therapeutic strategies for HCC. [ABSTRACT FROM AUTHOR]

Published
2023
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83. The role of ST2 and ST2 genetic variants in schistosomiasis

Author

Long, Xin, Daya, Michelle, Zhao, Jianping, Rafaels, Nicholas, Liang, Huifang, Potee, Joseph, Campbell, Monica, Zhang, Bixiang, Araujo, Maria Ilma, Oliveira, Ricardo R., Mathias, Rasika A., Gao, Li, Ruczinski, Ingo, Georas, Steve N., Vercelli, Donata, Beaty, Terri H., Barnes, Kathleen C., Chen, Xiaoping, and Chen, Qian

Published
2017
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88. Alkaline Phosphatase Combined with γ-Glutamyl Transferase is an Independent Predictor of Prognosis of Hepatocellular Carcinoma Patients Receiving Programmed Death-1 Inhibitors

Author

Xu, Lei, Chen, Lin, Zhang, Bin, Liu, Zhicheng, Liu, Qiumeng, Liang, Huifang, Chen, Yifa, Chen, Xiaoping, Leng, Chao, and Zhang, Bixiang

Subjects
Immunology, Immunology and Allergy
Abstract

BackgroundImmunotherapy plays an increasingly critical role in the systemic treatment of HCC. This current study aimed to establish a novel prognostic predictor of Programmed death 1 (PD-1) inhibitor therapy in hepatocellular carcinoma (HCC) independent of Child-Pugh grade.MethodsOur study screened patients with HCC who received PD-1 inhibitors at Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from January 2018 to December 2020. ALG grade was determined by the patient’s serum ALP and GGT levels before the initiation of PD-1 inhibitors. The endpoints of our study were overall survival (OS) and progression free survival (PFS). Follow-up ended at May 31, 2022.ResultsEighty- five patients (77 with Child−Pugh grade A, 8 with Child−Pugh grade B at baseline) were enrolled according to the inclusion criteria. Patients with Child−Pugh grade A achieved longer PFS and OS than those with Child−Pugh grade B. Patients with ALG grade 3 at baseline showed worse tumor response and poorer survival, and ALG grade could stratify patients with Child−Pugh grade A into subgroups with significantly different prognosis.ConclusionsALG grade, combining ALP and GGT, is a novel and readily available prognostic marker and the predictive effect of ALG grade on patient prognosis is independent of Child−Pugh grade.

Published
2022

89. [Corrigendum] High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer

Author

Liao, Zhibin, primary, Zhang, Hongwei, additional, Fan, Pan, additional, Huang, Qibo, additional, Dong, Keshuai, additional, Qi, Yongqiang, additional, Song, Jia, additional, Chen, Lin, additional, Liang, Huifang, additional, Chen, Xiaoping, additional, Zhang, Zhanguo, additional, and Zhang, Bixiang, additional

Published
2021
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91. High PLK4 expression promotes tumor progression and induces epithelial-mesenchymal transition by regulating the Wnt/β-catenin signaling pathway in colorectal cancer

Author

Liao, Zhibin, Zhang, Hongwei, Fan, Pan, Huang, Qibo, Dong, Keshuai, Qi, Yongqiang, Song, Jia, Chen, Lin, Liang, Huifang, Chen, Xiaoping, Zhang, Zhanguo, and Zhang, Bixiang

Subjects
Male, Cancer Research, Epithelial-Mesenchymal Transition, Carcinogenesis, Mice, Nude, colorectal cancer, Protein Serine-Threonine Kinases, Mice, Biomarkers, Tumor, metastasis, Animals, Humans, Wnt Signaling Pathway, Aged, Mice, Inbred BALB C, Articles, Middle Aged, Xenograft Model Antitumor Assays, digestive system diseases, Gene Expression Regulation, Neoplastic, polo-like kinase 4, Oncology, Lymphatic Metastasis, Disease Progression, Female, Colorectal Neoplasms, Corrigendum
Abstract

Polo-like kinase 4 (PLK4) has been identified as an oncogene, which is overexpressed in various types of human cancer; however, its role in colorectal cancer (CRC) development remains unknown. The present study demonstrated that PLK4 protein expression was upregulated in CRC tissues compared with in normal tissues through western blotting. In addition, immunohistochemical analysis of 39 CRC specimens further demonstrated that PLK4 protein expression was upregulated in 64.1% (25/39) of samples. Increased PLK4 expression was closely associated with enhanced tumor size (P=0.031), lymph node metastasis (P=0.016) and TNM stage (P=0.001). Subsequently, cell viability, wound scratch, migration and invasion assays were conducted in vitro, and nude mice CRC xenograft models were generated. The results demonstrated that knockdown of PLK4 in CRC cells resulted in significant decreases in cell viability and proliferation, and decreased the protein expression levels of N-cadherin and snail, which are biomarkers of epithelial-mesenchymal transition. Furthermore, PLK4 knockdown inactivated the Wnt/β-catenin pathway in CRC cells in vitro and in vivo, and suppressed the growth of xenograft tumors in nude mice. In conclusion, these results suggested that PLK4 may promote the carcinogenesis and metastasis of CRC, thus indicating that PLK4 may be considered a molecular target for CRC treatment.

Published
2021

100. H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen‐Activated Protein Kinase–Dependent Manner and Sponging microRNA 200b‐3p

Author

Huang, Zhao, primary, Chu, Liang, additional, Liang, Junnan, additional, Tan, Xiaolong, additional, Wang, Yu, additional, Wen, Jingyuan, additional, Chen, Jin, additional, Wu, Yu, additional, Liu, Sha, additional, Liao, Jingyu, additional, Hou, Rui, additional, Ding, Zeyang, additional, Zhang, Zhanguo, additional, Liang, Huifang, additional, Song, Shasha, additional, Yang, Caihong, additional, Zhang, Jinming, additional, Guo, Tao, additional, Chen, Xiaoping, additional, and Zhang, Bixiang, additional

Published
2021
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