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414 results on '"Kan, Quancheng"'

9. Regulation of microRNAs function by circular RNAs in human cancer

Author

Han, Chao, Seebacher, Nicole A, Hornicek, Francis J, Kan, Quancheng, and Duan, Zhenfeng

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Cancer, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, circRNA, miRNA, cancer, gene regulatory mechanisms, target therapy, Oncology and carcinogenesis
Abstract

Circular RNAs (circRNAs) are a newly validated class of endogenous non-coding RNA, generated from the ligation of exons, introns, or both, which arise via a diverse number of cellular mechanisms. Due to rapid advances in the development of combined high-throughput sequencing and bioinformatics analyzing tools, many circRNAs have recently been discovered, revealing an expansive number of ubiquitously expressed mammalian circRNAs. Interestingly, it has recently been confirmed that circRNAs bind to microRNAs (miRs), as miR "sponges", acting to suppress miR function. As miRs are known to alter the development and progression of cancer, circRNAs may offer a novel diagnostic and prognostic biomarker for cancer. Indeed, recent evidence has shown that circRNAs are associated with many human cancers. Herein, we review the molecular characteristics and biogenesis of circRNAs, with a focus on newly identified circRNAs that may play an important role in human cancer, through their regulation of miR expression.

Published
2017

12. NSUN2/YBX1 promotes the progression of breast cancer by enhancing HGH1 mRNA stability through m5C methylation.

Author

Zhang, Xuran, An, Ke, Ge, Xin, Sun, Yuanyuan, Wei, Jingyao, Ren, Weihong, Wang, Han, Wang, Yueqin, Du, Yue, He, Lulu, Li, Ouwen, Zhou, Shaoxuan, Shi, Yong, Ren, Tong, Yang, Yun-gui, Kan, Quancheng, and Tian, Xin

Subjects
RNA modification & restriction, BREAST cancer, ELONGATION factors (Biochemistry), GENE expression, RNA methylation, METHYLGUANINE
Abstract

Background: RNA m5C methylation has been extensively implicated in the occurrence and development of tumors. As the main methyltransferase, NSUN2 plays a crucial regulatory role across diverse tumor types. However, the precise impact of NSUN2-mediated m5C modification on breast cancer (BC) remains unclear. Our study aims to elucidate the molecular mechanism underlying how NSUN2 regulates the target gene HGH1 (also known as FAM203) through m5C modification, thereby promoting BC progression. Additionally, this study targets at preliminarily clarifying the biological roles of NSUN2 and HGH1 in BC. Methods: Tumor and adjacent tissues from 5 BC patients were collected, and the m5C modification target HGH1 in BC was screened through RNA sequencing (RNA-seq) and single-base resolution m5C methylation sequencing (RNA-BisSeq). Methylation RNA immunoprecipitation-qPCR (MeRIP-qPCR) and RNA-binding protein immunoprecipitation-qPCR (RIP-qPCR) confirmed that the methylation molecules NSUN2 and YBX1 specifically recognized and bound to HGH1 through m5C modification. In addition, proteomics, co-immunoprecipitation (co-IP), and Ribosome sequencing (Ribo-Seq) were used to explore the biological role of HGH1 in BC. Results: As the main m5C methylation molecule, NSUN2 is abnormally overexpressed in BC and increases the overall level of RNA m5C. Knocking down NSUN2 can inhibit BC progression in vitro or in vivo. Combined RNA-seq and RNA-BisSeq analysis identified HGH1 as a potential target of abnormal m5C modifications. We clarified the mechanism by which NSUN2 regulates HGH1 expression through m5C modification, a process that involves interactions with the YBX1 protein, which collectively impacts mRNA stability and protein synthesis. Furthermore, this study is the first to reveal the binding interaction between HGH1 and the translation elongation factor EEF2, providing a comprehensive understanding of its ability to regulate transcript translation efficiency and protein synthesis in BC cells. Conclusions: This study preliminarily clarifies the regulatory role of the NSUN2-YBX1-m5C-HGH1 axis from post-transcriptional modification to protein translation, revealing the key role of abnormal RNA m5C modification in BC and suggesting that HGH1 may be a new epigenetic biomarker and potential therapeutic target for BC. [ABSTRACT FROM AUTHOR]

Published
2024
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13. The emerging roles and therapeutic potential of cyclin-dependent kinase 11 (CDK11) in human cancer

Author

Zhou, Yubing, Shen, Jacson K, Hornicek, Francis J, Kan, Quancheng, and Duan, Zhenfeng

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Trials and Supportive Activities, Clinical Research, Breast Cancer, Cancer, Genetics, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Aetiology, Apoptosis, Breast Neoplasms, Cell Cycle, Cell Proliferation, Cyclin-Dependent Kinases, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Genetic Therapy, Humans, Liposarcoma, Multiple Myeloma, Neoplasms, Osteosarcoma, Phosphorylation, Piperazines, Protein Serine-Threonine Kinases, Pyridines, RNA Splicing, Treatment Outcome, CDK11, CDKs inhibitor, cell cycle, therapeutic target, cancer therapy, Oncology and carcinogenesis
Abstract

Overexpression and/or hyperactivation of cyclin-dependent kinases (CDKs) are common features of most cancer types. CDKs have been shown to play important roles in tumor cell proliferation and growth by controlling cell cycle, transcription, and RNA splicing. CDK4/6 inhibitor palbociclib has been recently approved by the FDA for the treatment of breast cancer. CDK11 is a serine/threonine protein kinase in the CDK family and recent studies have shown that CDK11 also plays critical roles in cancer cell growth and proliferation. A variety of genetic and epigenetic events may cause universal overexpression of CDK11 in human cancers. Inhibition of CDK11 has been shown to lead to cancer cell death and apoptosis. Significant evidence has suggested that CDK11 may be a novel and promising therapeutic target for the treatment of cancers. This review will focus on the emerging roles of CDK11 in human cancers, and provide a proof-of-principle for continued efforts toward targeting CDK11 for effective cancer treatment.

Published
2016

17. VTE Risk Profiles and Prophylaxis in Medical and Surgical Inpatients: The Identification of Chinese Hospitalized Patients’ Risk Profile for Venous Thromboembolism (DissolVE-2)—A Cross-sectional Study

Author

Zhu, Fuyi, Jiang, Min, Deng, Yingmei, Li, Xueqii, Geng, Deqin, Zhai, Jieming, Wang, Caifang, Zhang, Junhui, Cao, Jie, Chen, Shaoyong, Li, Gangzhi, Wang, Liming, Zhang, Yulin, Liu, Xiang, Zhang, Xiaoju, Luo, Xianguo, Li, Xia, Zhao, Li, Zu, Nanwei, Lu, Xiaofang, Yang, Lan, Zhang, Nuofu, Pang, Wuyan, Ji, Yingqun, Yao, Yazhou, Sun, Xuhui, Xu, Wenda, Zhao, Jianqing, Leng, Huilin, Yu, Zehong, Kuang, Guangzhi, Huang, Yijiang, Chen, Lin, Shi, Juhong, Xin, Shijie, Xiao, Peng, Du, Zhiming, Wei, Yan, Liu, Yongchun, Zhang, Chunfang, Xu, Yvming, Yang, Zhou, Liu, Ruijuan, Liu, Yiheng, Chen, Yan, Qin, Jin, Liu, Side, Zhou, Hui, Zhang, Zhuo, Wei, Liping, Ren, Tao, Wang, Baojun, Chen, Hong, Mao, Guozhang, Ying, Yinghua, Ding, Guoxian, Dui, Danhua, Du, Taiping, Li, Xichun, Lu, Jie, Zheng, Defu, He, Tao, Zhai, Zhenguo, Kan, Quancheng, Li, Weimin, Qin, Xinyu, Qu, Jieming, Shi, Yuankai, Xu, Ruihua, Xu, Yuming, Zhang, Zhu, and Wang, Chen

Published
2019
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35. RNA Structural Dynamics Modulate EGFR-TKI Resistance Through Controlling YRDCTranslation in NSCLC Cells

Author

Shi, Boyang, An, Ke, Wang, Yueqin, Fei, Yuhan, Guo, Caixia, Cliff Zhang, Qiangfeng, Yang, Yun-Gui, Tian, Xin, and Kan, Quancheng

Abstract

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) positively affect the initial control of non-small cell lung cancer(NSCLC). Rapidly acquired resistance to EGFR-TKIs is a major hurdle in successful treatment. However, the mechanisms that control the resistance of EGFR-TKIs remain largely unknown. RNA structureshave widespread and crucial functions in many biological regulations; however, the functions of RNA structures in regulating cancer drug resistance remain unclear. Here, the psoralen analysis of RNA interactions and structures (PARIS) method is used to establish the higher-order RNA structure maps of EGFR-TKIs-resistant and -sensitive cells of NSCLC. Our results show that RNA structural regions are enriched in untranslated regions (UTRs) and correlate with translation efficiency (TE). Moreover, yrdC N6-threonylcarbamoyltransferase domain containing(YRDC) promotes resistance to EGFR-TKIs. RNA structure formation in YRDC3′ UTR suppresses embryonic lethal abnormal vision-like 1 (ELAVL1) binding, leading to EGFR-TKI sensitivity by impairing YRDCtranslation. A potential therapeutic strategy for cancer treatment is provided using antisense oligonucleotide (ASO) to perturb the interaction between RNA and protein. Our study reveals an unprecedented mechanism through which the RNA structure switch modulates EGFR-TKI resistanceby controlling YRDCmRNA translation in an ELAVL1-dependent manner.

Published
2023
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39. The Heterogeneity of Immune Cell Infiltration Landscape and Its Immunotherapeutic Implications in Hepatocellular Carcinoma

Author

Guo, Yuanyuan, Yang, Jing, Ren, Kaidi, Tian, Xueke, Gao, Hua, Tian, Xin, Zhang, Xiaojian, and Kan, Quancheng

Subjects
Gene Expression Regulation, Neoplastic, Carcinoma, Hepatocellular, Liver Neoplasms, Mutation, Immunology, Biomarkers, Tumor, Tumor Microenvironment, Humans, Immunology and Allergy, Immunotherapy
Abstract

Immunotherapy, closely associated with immune infiltration and tumor mutation burden (TMB), is emerging as a promising strategy for treating tumors, but its low response rate in hepatocellular carcinoma (HCC) remains a major challenge. Herein, we applied two algorithms to uncover the immune infiltration landscape of the immune microenvironment in 491 HCC patients. Three immune infiltration patterns were defined using the CIBERSORT method, and the immune cell infiltration (ICI) scores were established using principal component analysis. In the high ICI score group, the activation of the Wnt/β-catenin pathway was significantly enriched and expressions of immune checkpoint genes increased, which showed a pessimistic outcome. The low ICI score group was characterized by increased TMB and enrichment of metabolism-related pathways. Further analysis found that the ICI score exhibited a significant difference in age ≥65/age

Published
2022

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