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| 1 | Circular RNA is enriched and stable in exosomes: a promising biomarker for cancer diagnosis显示文摘 | Yan Li Qiupeng Zheng Chunyang Bao Shuyi Li Weijie Guo Jiang Zhao Di Chen Jianren Gu Xianghuo He Shenglin Huang | 2015 | Cell Research2015，25，8： | 323 |
| 2 | microRNAs: tiny RNA molecules, huge driving forces to move the cell显示文摘Cell migration or movement is a highly dynamic cellular process,requiring precise regulation that is essential for a variety of biological processes.microRNAs(miRNAs)are a class of tiny non-coding RNA molecules that function as critical post-transcriptional regulators of gene expression.Emerging evidence demonstrates that miRNAs play important roles in cell migration and directly contribute to extracellular matrix(ECM)remodeling,cell adhesion,and cell signalling that controls cell migration by targeting a large number of protein-coding genes.Accordingly,the dysregulation of these miRNAs has been linked to several migration-related diseases.In this review,we summarize and highlight the recent advances concerning the roles and validated targets of miRNAs in the control of cell movement. | Shenglin Huang Xianghuo He | 2010 | Protein & Cell2010，1，10： | 3 |
| 3 | miR-27b synergizes with anticancer drugs via p53 activation and CYPIB1 suppression显示文摘 | Wenjing Mu Chaobo Hu Haibin Zhang Zengqiang Qu Jin Cen Zhixin Qiu Chao Li Haozhen Ren Yixue Li Xianghuo He Xiaolei Shi Lijian Hui | 2015 | Cell Research2015，25，4： | 3 |
| 4 | Amplification of MPZL1/PZR promotes tumor cell migration through Src-mediated phosphorylation of cortactin in hepatocellular carcinoma显示文摘我们以前在 hepatocellular 癌(HCC ) 识别了体的拷贝数字改变(CNA ) 的 1 241 个区域。在现在的学习,我们发现那新奇周期性的焦点的 amplicon, 1q24.1-24.2,在 HCC 指向 MPZL1 基因。尤其是,在 MPZL1 和 HCC 标本的 intrahepatic 转移的表示层次之间有积极关联。MPZL1 能显著地提高 HCC 房间的迁移、变形的潜力。而且,我们发现 MPZL1 由支持 HCC 房间移植的机制之一由导致支持 metastatic 蛋白质的 phosphorylation 和激活, cortactin。另外,我们发现 Src kinase 调停 cortactin 的 phosphorylation 和激活由 MPZL1 overexpression 导致了。一起拿,这些调查结果建议 MPZL1 是拷贝数字扩大的一个周期性的区域在 HCC 目标为 1q24.1-24.2 的新奇支持 metastatic 基因。 | Deshui Jia Ying Jing Zhenfeng Zhang Li Liu Jie Ding Fangyu Zhao Chao Ge Qifeng Wang Taoyang Chen Ming Yao Jinjun Li Jianren Gu Xianghuo He | 2014 | Cell Research2014，24，2： | 2 |
| 5 | Choline Transporters in Human Lung Adenocarcinoma: Expression and Functional Implications显示文摘然而,胆碱是为房间幸存和增长的必要营养素胆碱运输 ers 的表示和功能很好没在癌症被识别。在这研究,我们检测了 mRNA 和器官的阳离子 transporter 的蛋白质表示 OCT3,肉毒碱 / 阳离子运输 ers OCTN1 和 OCTN2,和在人的肺腺癌房间的像运输的 proteinCTL1 衬里的胆碱 A549, H1299 和 SPC-A-1.Their 表示模式是进一步的在 25 人的主要腺癌纸巾证实了。在这些房间线的胆碱举起被 CTL1 禁止者显著地堵住,但是仅仅部分在房间增长上由 10 月或这些禁止者的 OCTNinhibitors.The 功效禁止了密切与他们堵住胆碱运输的能力被相关。在这些运输 ers 的本国的表示下面,全部的胆碱举起被特定的 PI3K/AKT 禁止者显著地堵住。这些结果在人的肺腺癌的房间增长描述胆碱运输 ers 和他们的相关功能的表示,因此提供潜在的“胆碱饥饿”通过指向胆碱运输 ers 的癌症干扰的策略,特别 CTL1。 | Tao WANG Jinjun LI Fei CHEN Yingjun ZHAO Xianghuo HE Dafang WAN Jianren GU | 2007 | Acta Biochimica et Biophysica Sinica2007，39，9： | 1 |
| 6 | Application of third-generation sequencing in cancer research显示文摘In the past several years,nanopore sequencing technology from Oxford Nanopore Technologies(ONT)and single-molecule real-time(SMRT)sequencing technology from Pacific BioSciences(PacBio)have become available to researchers and are currently being tested for cancer research.These methods offer many advantages over most widely used high-throughput short-read sequencing approaches and allow the comprehensive analysis of transcriptomes by identifying full-length splice isoforms and several other posttranscriptional events.In addition,these platforms enable structural variation characterization at a previously unparalleled resolution and direct detection of epigenetic marks in native DNA and RNA.Here,we present a comprehensive summary of important applications of these technologies in cancer research,including the identification of complex structure variants,alternatively spliced isoforms,fusion transcript events,and exogenous RNA.Furthermore,we discuss the impact of the newly developed nanopore direct RNA sequencing(RNA-Seq)approach in advancing epitranscriptome research in cancer.Although the unique challenges still present for these new singlemolecule long-read methods,they will unravel many aspects of cancer genome complexity in unprecedented ways and present an encouraging outlook for continued application in an increasing number of different cancer research settings. | Zhiao Chen Xianghuo He | 2021 | Medical Review2021，1，2： | 1 |
| 7 | Dysfunction of Murine Dendritic Cells Induced by Incubation with Tumor Cells显示文摘In vivo studies showed that dendritic cell (DC) dysfunction occurred in tumor microenvironment. As tumors were composed of many kinds of cells,the direct effects of tumor cells on immature DCs (imDCs) are needed for further studies in vitro. In the present study,bone marrow-derived imDCs were incubated with lymphoma,hepatoma and menaloma cells in vitro and surface molecules in imDCs were determined by flow cytometry. Then,imDCs incubated with tumor cells or control imDCs were further pulsed with tumor lysates and then incubated with splenocytes to perform mixed lymphocyte reaction. The DC-dependent tumor antigen-specific T cell proliferation,and IL-12 secretion were determined by flow cytometry,and enzyme-linked immunosorbent assay respectively. Finally,the DC-dependent tumor-associated antigen-specific CTL was determined by enzyme-linked immunospot assay. The results showed that tumor cell-DC incubation down-regulated the surface molecules in imDCs,such as CD80,CD54,CD11b,CD11a and MHC class Ⅱ molecules. The abilities of DC-dependent antigen-specific T cell proliferation and IL-12 secretion were also decreased by tumor cell incubation in vitro. Most importantly,the ability for antigenic-specific CTL priming of DCs was also decreased by incubation with tumor cells. In the present in vitro study demonstrated that the defective abilities of DCs induced by tumor cell co-incubation and the co-incubation system might be useful for future study of tumor-immune cells direct interaction and for drug screen of immune-modulation. | Fengguang Gao Xin Hui Xianghuo He Dafang Wan Jianren Gu | 2008 | Cellular & Molecular Immunology2008，5，2： | 0 |
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