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Your search keyword '"Guan, Xin-Yuan"' showing total 721 results
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721 results on '"Guan, Xin-Yuan"'

12. Roles of heat shock proteins in tumor immune microenvironment

Author

Zhou Qin, Guan Xin-Yuan, and Li Yan

Subjects
heat shock proteins, tumor microenvironment, immune cells, vasculature, Medicine
Abstract

Heat shock proteins (HSPs) are the most abundant molecular chaperones in cells, categorized based on function and molecular weight into HSP families, namely, HSP40, HSP70, HSP90, HSP110, and HSPB (heat shock protein B), et al. HSPs are involved in protein homeostasis by assisting in the correct folding of proteins or incorrectly folded proteins, refolding partially denatured proteins, and degrading damaged proteins. High levels of HSPs have been shown to participate in oncogenesis, progression, and chemotherapy resistance in many cancers. Recently a new range of functions besides chaperons, mostly in modulation of immune responses, have been shown for these extracellular HSPs. Here, we review the interactions between the HSPs and different immune cells, such as T lymphocytes, B cells, dendritic cells, macrophages, NK cells, and myeloid suppressor cells in the tumor microenvironment, as well as tumor vasculature and angiogenesis in tumor formation. The underlying mechanisms of HSPs’ regulation on immune response in tumor microenvironments are also discussed. The understanding of new functions of HSPs in tumor microenvironment may provide critical insights for the development of effective immunotherapies.

Published
2024
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24. The RARS–MAD1L1 Fusion Gene Induces Cancer Stem Cell–like Properties and Therapeutic Resistance in Nasopharyngeal Carcinoma

Author

Zhong, Qian, Liu, Zhi-Hua, Lin, Zhi-Rui, Hu, Ze-Dong, Yuan, Li, Liu, Yan-min, Zhou, Ai-Jun, Xu, Li-Hua, Hu, Li-Juan, Wang, Zi-Feng, Guan, Xin-Yuan, Hao, Jia-Jie, Lui, Vivian WY, Guo, Ling, Mai, Hai-Qiang, Chen, Ming-Yuan, Han, Fei, Xia, Yun-Fei, Grandis, Jennifer R, Zhang, Xing, and Zeng, Mu-Sheng

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Dental/Oral and Craniofacial Disease, Stem Cell Research, Genetics, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Arginine-tRNA Ligase, Biomarkers, Tumor, Cell Cycle Proteins, Cell Line, Tumor, Disease Models, Animal, Drug Resistance, Neoplasm, Gene Knockdown Techniques, Gene Rearrangement, Humans, In Situ Hybridization, Fluorescence, Mice, Nasopharyngeal Carcinoma, Neoplastic Stem Cells, Nuclear Proteins, Oncogene Proteins, Fusion, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins c-myc, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

Purpose: Nasopharyngeal carcinoma (NPC) is the most common head and neck cancer in Southeast Asia. Because local recurrence and distant metastasis are still the main causes of NPC treatment failure, it is urgent to identify new tumor markers and therapeutic targets for advanced NPC.Experimental Design: RNA sequencing (RNA-seq) was applied to look for interchromosome translocation in NPC. PCR, FISH, and immunoprecipitation were used to examine the fusion gene expression at RNA, DNA, and protein levels in NPC biopsies. MTT assay, colony formation assay, sphere formation assay, co-immunoprecipitation, chromatin immunoprecipitation assay, and in vivo chemoresistance assay were applied to explore the function of RARS-MAD1L1 in NPC.Results: We demonstrated that RARS-MAD1L1 was present in 10.03% (35/349) primary NPC biopsies and 10.7% (9/84) in head and neck cancer (HNC) samples. RARS-MAD1L1 overexpression increased cell proliferation, colony formation, and tumorigenicity in vitro, and the silencing of endogenous RARS-MAD1L1 reduced cancer cell growth and colony formation in vitro In addition, RARS-MAD1L1 increased the side population (SP) ratio and induced chemo- and radioresistance. Furthermore RARS-MAD1L1 interacted with AIMP2, which resulted in activation of FUBP1/c-Myc pathway. The silencing of FUBP1 or the administration of a c-Myc inhibitor abrogated the cancer stem cell (CSC)-like characteristics induced by RARS-MAD1L1. The expression of c-Myc and ABCG2 was higher in RARS-MAD1L1-positive HNC samples than in negative samples.Conclusions: Our findings indicate that RARS-MAD1L1 might contribute to tumorigenesis, CSC-like properties, and therapeutic resistance, at least in part, through the FUBP1/c-Myc axis, implying that RARS-MAD1L1 might serve as an attractive target for therapeutic intervention for NPC. Clin Cancer Res; 24(3); 659-73. ©2017 AACR.

Published
2018

25. A hepatocyte differentiation model reveals two subtypes of liver cancer with different oncofetal properties and therapeutic targets

Author

Liu, Ming, Yan, Qian, Sun, Yi, Nam, Yoonhee, Hu, Liang, Loong, Jane HC, Ouyang, Qi, Zhang, Yu, Li, Hao-Long, Kong, Fan-En, Li, Lei, Li, Mei-Mei, Cheng, Wei, Jiang, Ling-Xi, Fang, Shuo, Yang, Xiao-Dong, Mo, Jia-Qiang, Gong, Yuan-Feng, Tang, Yun-Qiang, Li, Yan, Yuan, Yun-Fei, Ma, Ning-Fang, Lin, Ge, Ma, Stephanie, Wang, Ji-Guang, and Guan, Xin-Yuan

Published
2020

30. A neural‐related gene risk score for head and neck squamous cell carcinoma.

Author

Tao, Zhuo‐ying, Yang, Wei‐fa, Zhu, Wang‐yong, Wang, Lei‐lei, Li, Kar Yan, Guan, Xin‐yuan, and Su, Yu‐xiong

Subjects
STATISTICS, IMMUNE checkpoint inhibitors, PREDICTIVE tests, HEAD & neck cancer, REGRESSION analysis, RISK assessment, T-test (Statistics), GENE expression profiling, SURVIVAL analysis (Biometry), KAPLAN-Meier estimator, CHI-squared test, DESCRIPTIVE statistics, RESEARCH funding, DATA analysis, SQUAMOUS cell carcinoma, PROPORTIONAL hazards models, OVERALL survival, IMMUNOTHERAPY
Abstract

Objectives: This study aimed to establish a neural‐related gene risk score (NRGRS) for the prediction of head and neck squamous cell carcinoma prognosis and explore its predictive value on the benefit of immune checkpoint inhibitor therapy. Methods: Based on the transcriptome data of HNSCC patients (n = 546) from The Cancer Genome Atlas database, 37 neural‐related hub genes were identified by weighted gene co‐expression network analysis. Four genes (ITGA5, PYGM, GNG7 and ATP2A3) were identified to construct NRGRS using Lasso‐Cox regression method based on the derivation cohort and validated in the Gene Expression Omnibus cohort (n = 109). The survival analysis was performed to validate the prognostic value of NRGRS and immune characteristics in NRGRS‐defined subgroups were analyzed. Results: NRGRS‐high patients had a worse overall survival than NRGRS‐low patients. Tumors with high NRGRS were more likely to have high infiltration of naive CD4+ T cells, M0, M2 macrophages and resting mast cells, which illustrated suppressive immunity and less benefit from immunotherapy therapy. Conclusion: NRGRS strongly correlates with survival and is a promising biomarker to predict immunotherapy benefits for head and neck cancer patients. This study provides evidence for the potential correlation between neural‐related transcriptome alteration and immune activity. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Comprehensive single-cell sequencing reveals the stromal dynamics and tumor-specific characteristics in the microenvironment of nasopharyngeal carcinoma

Author

Gong, Lanqi, Kwong, Dora Lai-Wan, Dai, Wei, Wu, Pingan, Li, Shanshan, Yan, Qian, Zhang, Yu, Zhang, Baifeng, Fang, Xiaona, Liu, Li, Luo, Min, Liu, Beilei, Chow, Larry Ka-Yue, Chen, Qingyun, Huang, Jinlin, Lee, Victor Ho-Fun, Lam, Ka-On, Lo, Anthony Wing-Ip, Chen, Zhiwei, Wang, Yan, Lee, Anne Wing-Mui, and Guan, Xin-Yuan

Published
2021
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50. Loss of ESRP2 Activates TAK1‐MAPK Signaling through the Fetal RNA‐Splicing Program to Promote Hepatocellular Carcinoma Progression.

Author

Yan, Qian, Fang, Xiaona, Liu, Xiaoxia, Guo, Sai, Chen, Siqi, Luo, Min, Lan, Ping, and Guan, Xin‐Yuan

Subjects
HEPATOCELLULAR carcinoma, ALTERNATIVE RNA splicing, RNA splicing, CARCINOEMBRYONIC antigen, IMMUNE checkpoint proteins, GENE expression
Abstract

Tumors usually display fetal‐like characteristics, and many oncofetal proteins have been identified. However, fetal‐like reprogramming of RNA splicing in hepatocellular carcinoma (HCC) is poorly understood. Here, it is demonstrated that the expression of epithelial splicing regulatory protein 2 (ESRP2), an RNA splicing factor, is suppressed in fetal hepatocytes and HCC, in parallel with tumor progression. By combining RNA‐Seq with splicing analysis, it is identified that ESRP2 controls the fetal‐to‐adult switch of multiple splice isoforms in HCC. Functionally, ESRP2 suppressed cell proliferation and migration by specifically switching the alternative splicing (AS) of the TAK1 gene and restraining the expression of the fetal and oncogenic isoform, TAK1_ΔE12. Notably, aberrant TAK1 splicing led to the activation of p38MAPK signaling and predicted poor prognosis in HCC patients. Further investigation revealed that TAK1_ΔE12 protein interacted closely with TAB3 and formed liquid condensation in HCC cells, resulting in p38MAPK activation, enhanced cell migration, and accelerated tumorigenesis. Loss of ESRP2 sensitized HCC cells to TAK1 kinase inhibitor (TAK1i), promoting pyroptotic cell death and CD8+ T cell infiltration. Combining TAK1i with immune checkpoint therapy achieved potent tumor regression in mice. Overall, the findings reveal a previously unexplored onco‐fetal reprogramming of RNA splicing and provide novel therapeutic avenues for HCC. [ABSTRACT FROM AUTHOR]

Published
2024
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