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| 1 | HIF-1α-induced expression of m6A reader YTHDF1 drives hypoxia-induced autophagy and malignancy of hepatocellular carcinoma by promoting ATG2A and ATG14 translation显示文摘N6-methyladenosine(m6A),and its reader protein YTHDF1,play a pivotal role in human tumorigenesis by affecting nearly everystage of RNA metabolism.Autophagy activation is one of the ways by which cancer cells survive hypoxia.However,the possibleinvolvement of m6A modification of mRNA in hypoxia-induced autophagy was unexplored in human hepatocellular carcinoma(HCO).In this study,specific variations in YTHDF1 expression were detected in YTHDF1-overexpressing,knockout,and-knockdownHCC cells,HCC organoids,and HCC patient-derived xenograft(PDX)murine models.YTHDF1 expression and hypoxia inducedautophagy were significantly correlated in vitro;signifhcant overexpression of YTHDF1 in HCC tissues was associated with poorprognosis,Multivariate cox regression analysis identihed YTHDF1 expression as an independent prognostic factor in patients withHCC.Multiple HC models conhrmed that YTHDF1 deficiency inhibited HCC autophagy,growth,and metastasis.Luciferase reporterassays and chromatin immunoprecipitation demonstrated that HlIF-1a regulated YTHDF1 transcription by directly binding to itspromoter region under hypoxia.The results of methylated RNA immunoprecipitation sequencing,proteomics,and polysomeprofling indicated that YTHDF1 contibuted to the translation of autophagy-related genes ATG2A and ATG14 by binding to m6A-modifhed ATG2A and ATG14 mRNA,thus facilitating autophagy and autophagy-related malignancy of HCC.Taken together,HlE-1d-induced YTHDF1 expression was associated with hypoxia-induced autophagy and autophagy-related HCC progression via promoting translation of autophagy-related genes ATG2A and ATG14 in a m6A-dependent manner.Our fndings suggest thatYTHDF1 is a potential prognostic biomarker and therapeutic target for patients with HCC. | Qing Li Yong Ni Liren Zhang Runqiu Jiang Jing Xu Hong Yang Yuanchang Hu Jiannan Qiu Liyong Pu Jinhai Tang Xuehao Wang | 2021 | Signal Transduction and Targeted Therapy2021，6，3： | 24 |
| 2 | Interleukin-33 drives hepatic fibrosis through activation of hepatic stellate cells显示文摘Liver fibrosis is a consequence of chronic liver disease,causing morbidity and mortality.Interleukin-33(IL-33)is a critical mediator of inflammation,which may be involved in the development of liver fibrosis.Here,we investigated the role of IL-33 in human patients and experimental bile-duct ligation(BDL)-induced fibrosis in mice.We report increased hepatic IL-33 expression in the murine BDL model of fibrosis and in surgical samples obtained from patients with liver fibrosis.Liver injury,inflammatory cell infiltration and fibrosis were reduced in the absence of the IL-33/ST2 receptor,and the activation of hepatic stellate cells(HSCs)was decreased in ST2-deficient mice.Recombinant IL-33 activated HSCs isolated from C57BL/6 mice,leading to the expression of IL-6,TGF-β,α-SMA and collagen,which was abrogated in the absence of ST2 or by pharmacological inhibition of MAPK signaling.Finally,administration of recombinant IL-33 significantly increased hepatic inflammation in sham-operated BL6 mice but did not enhance BDL-induced hepatic inflammation and fibrosis.In conclusion,BDL-induced liver inflammation and fibrosis are dependent on ST2 signaling in HSCs,and therefore,the IL-33/ST2 pathway may be a potential therapeutic target in human patients with chronic hepatitis and liver fibrosis. | Zhongming Tan Qianghui Liu Runqiu Jiang Long Lv Siamak S Shoto Isabelle Maillet Valerie Quesniaux Junwei Tang Wenjie Zhang Beicheng Sun Bernhard Ryffel | 2018 | Cellular & Molecular Immunology2018，15，4： | 24 |
| 3 | IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation显示文摘 | Zhongming Tan Xiaofeng Qian Runqiu Jiang Qianghui Liu Youjing Wang Chen Chen Xuehao Wang Bernhard Ryffel Beicheng Sun | 2013 | The Journal of Immunology2013，，4： | 2 |
| 4 | Long-term Hardening Characteristics of Prestressed Anchorage Grout显示文摘Grout plays an important role in the transmission and maintenance of anchoring force,and in the protection of anchorage materials against corrosion.Thus,the hardening characteristics of grout directly affect the anchoring effectivity and long-term reliability.We have excavated a prestressed anchorage which has been in service for 20 years,and have tested the grout which has worked for that long period under complicated geological conditions through strength tests and have analyzed its mineral composition using scanning electron microscopy(SEM) and X-ray diffraction(XRD).The results show that the mineral composition of the 12.5 m segment differs from other segments,and corresponds with poor coagulation characteristics of the 12.5 m segment grout.Analysis shows that unhydrated tricalcium silicate may be the reason for the localized poor coagulation. | WANG Sheng CHEN Liyi HUANG Runqiu JIANG Zhaoqun WANG Yanshu | 2012 | Journal of Mountain Science2012，9，6： | 2 |
| 5 | TOX deficiency facilitates the differentiation of IL-17A-producingγδT cells to drive autoimmune hepatitis显示文摘The specification of theαβ/γδlineage and the maturation of medullary thymic epithelial cells(mTECs)coordinate central tolerance to self-antigens.However,the mechanisms underlying this biological process remain poorly clarified.Here,we report that dual-stage loss of TOX in thymocytes hierarchically impaired mTEC maturation,promoted thymic IL-17A-producingγδT-cell(Tγδ17)lineage commitment,and led to the development of fatal autoimmune hepatitis(AIH)via different mechanisms.Transfer ofγδT cells from TOX-deficient mice reproduced AIH.TOX interacted with and stabilized the TCF1 protein to maintain the balance ofγδT-cell development in thymic progenitors,and overexpression of TCF1 normalizedαβ/γδlineage specification and activation.In addition,TOX expression was downregulated inγδT cells from AIH patients and was inversely correlated with the AIH diagnostic score.Our findings suggest multifaceted roles of TOX in autoimmune control involving mTEC and Tγδ17 development and provide a potential diagnostic marker for AIH. | Qifeng He Yijun Lu Wenfang Tian Runqiu Jiang Weiwei Yu Yong Liu Meiling Sun Fei Wang Haitian Zhang Ning Wu Zhongjun Dong Beicheng Sun | 2022 | Cellular & Molecular Immunology2022，19，10： | 1 |
| 6 | IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation显示文摘 | Zhongming Tan Xiaofeng Qian Runqiu Jiang Qianghui Liu Youjing Wang Chen Chen Xuehao Wang Bernhard Ryffel Beicheng Sun | 2013 | The Journal of Immunology2013，，4： | 1 |
| 7 | Seismic energy dispersion compensation by multi-scale morphology显示文摘Seismic energy decays while propagating subsurface, which may reduce the resolution of seismic data. This paper studies the method of seismic energy dispersion compensation which provides the basic principles for multi-scale morphology and the spectrum simulation method. These methods are applied in seismic energy compensation. First of all, the seismic data is decomposed into multiple scales and the effective frequency bandwidth is selectively broadened for some scales by using a spectrum simulation method. In this process, according to the amplitude spectrum of each scale, the best simulation range is selected to simulate the middle and low frequency components to ensure the authenticity of the simulation curve which is calculated by the median method, and the high frequency component is broadened. Finally, these scales are reconstructed with reasonable coefficients, and the compensated seismic data can be obtained. Examples are shown to illustrate the feasibility of the energy compensation method. | Yu Junqing Wang Runqiu Liu Taoran Zhang Zhenglong Wu Jian Jiang Yongyong Sun Lipeng Xia Pei | 2014 | Petroleum Science2014，11，3： | 0 |
| 8 | A bystander cell-based GM-CSF secreting vaccine synergized with a low dose of cyclophosphamide presents therapeutic immune responses against murine hepatocellular carcinoma显示文摘Granulocyte 巨噬细胞刺激殖民地的因素(GM-CSF ) secreting 细胞的肿瘤疫苗在鼠科的模型和病人受不了癌症贡献有势力 antitumor 免疫者回答的正式就职。Hepatocellular 癌(HCC ) 是在中国的最经常、恶意的癌症之一。第一次,我们描述释放向与这类癌症作斗争代表步的疫苗的策略的 GM-CSF。在这研究,一个旁观者对鼠科的 HCC 的基于房间的 GM-CSF secreting 疫苗, Hepa1-6/B78H1-GM-CSF,与 cyclophosphamide (CY ) 的低剂量被共同管理。在与肿瘤和种痘质问以后,免疫学的试金证明细胞的 antitumor 免疫者回答高效地被激活并且肿瘤开发显著地被延迟,它依赖于有 CY 的协同作用。在鼠科的模型的 anti-HCC 疫苗的有希望的结果表明未来的可行性为在 HCC 病人的这治疗的临床的申请。 | Chen Chen Jiajie Hou Zhe Lin Ming Yao Runqiu Jiang Youjing Wang Yun Gao Qing Shao Lei Deng Yun Chen Beicheng Sun | 2013 | Cellular & Molecular Immunology2013，10，4： | 0 |
| 9 | PTPROt maintains T cell immunity in the microenvironment of hepatocellular carcinoma显示文摘Intratumoral T cells play a central role in anti-tumor immunity,and the balance between T effector cells(Teff)and regulatory T cells(Treg)affects the prognosis of cancer patients.However,educated by tumor microenvironment,T cells frequently fail in their responsibility.In this study,we aimed to investigate the role of truncated isoform of protein tyrosine phosphatase receptor-typeO(PTPROt)in T cell-mediated anti-tumor immunity.We recruited 70 hepatocellular carcinoma(HCC)patients and 30 healthy volunteers for clinical investigation,and analyzed cellular tumor immunity by using ptpro^(-/-) C57BL/6 mice and NOD/SCID mice.PTPROt expression was significantly downregulated in human HCC-infiltrating T cells due to the hypoxia microenvironment;PTPROt expression highly correlated with the intratumoral Teff/Treg ratio and clinicopathologic characteristics.Moreover,PTPROt deficiency attenuated T cell-mediated anti-tumor immunity and remarkably promoted mouse HCC growth.Mechanistically,deletion of PTPROt decreased Teff quantity and quality through phosphorylation of lymphocyte-specific tyrosine kinase,but increased Treg differentiation through phosphorylation of signal transducer and activator of transcription 5.In support of the Teff/Treg homeostasis,PTPROt serves as an important tumor suppressor in HCC microenvironment. | Jiajie Hou Lei Deng Han Zhuo Zhe Lin Yun Chen Runqiu Jiang Dianyu Chen Xudong Zhang Xingxu Huang Beicheng Sun | 2015 | Journal of Molecular Cell Biology2015，7，4： | 0 |
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