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| 1 | Blocking the recruitment of naive CD4+ T cells reverses immunosuppression in breast cancer显示文摘渗入肿瘤的 Tregs 的起源,肿瘤免疫力的抑制的批评调停人,是不清楚的。这里,,我们证明在人的乳癌的渗入肿瘤的天真的 CD4 + T 房间和 Tregs 有重叠 TCR 全部剧目几乎别与传播 Tregs 重叠,建议 intratumoral Tregs 主要在 situ 而非从招募的 Tregs 从天真的 T 房间发展。而且,许多天真的 CD4 + T 房间和 Tregs 密切被相关,两个显示的穷人为乳癌病人的预后。天真的 CD4 + T 房间与许多生产 CCL18 巨噬细胞成比例遵守肿瘤片。而且,采纳地转移的人的天真的 CD4 + T 房间以一种 CCL18 依赖的方式渗入人的乳癌 orthotopic 异种皮移植。在在人性化的鼠标的人的乳癌异种皮移植,由将 PITPNM3 的表达式击倒堵住天真的 CD4 + T 房间的招募进肿瘤, CCL18 受体,显著地减少 intratumoral Tregs 并且禁止肿瘤前进。这些调查结果建议那个乳房渗入肿瘤的 Tregs 从在 situ 区分进 Tregs 的传播天真的 CD4 + T 房间的趋化性产生。由防碍 CCL18 的 PITPNM3 识别禁止天真的 CD4 + T 房间招募进肿瘤可以是为 anticancer 免疫疗法的吸引人的策略。 | Shicheng Su Jianyou Liao Jiang Liu Di Huang Chonghua He Fei Chen LinBing Yang Wei Wu Jianing Chen Ling Lin Yunjie Zeng Nengtai Ouyang Xiuying Cui Herui Yao Fengxi Su Jian-dong Huang Judy Lieberman Qiang Liu Erwei Song | 2017 | Cell Research2017，27，4： | 19 |
| 2 | Overexpressed Cyclin D1 and CDK4 proteins are responsible for the resistance to CDK4/6 inhibitor in breast cancer that can be reversed by PI3K/mTOR inhibitors显示文摘CDK4/6 inhibitors are the standard treatment in advanced HR+/HER2-breast cancer patients.Nevertheless,the resistance to CDK4/6 inhibitors is inevitable and the strategies to overcome resistance are of great interest.Here,we show that the palbociclibresistant breast cancer cells expressed significantly higher levels of Cyclin D1 and CDK4 proteins because of upregulated protein synthesis.Silencing Cyclin D1 or CDK4 led to cell cycle arrest while silencing Cyclin E1 or CDK2 restored the sensitivity to palbociclib.Furthermore,PI3K/mTOR pathway was hyper-activated in palbociclib-resistant cells,leading to more phosphorylated 4E-BP1 and higher levels of Cyclin D1 and CDK4 translation.Targeting PI3K/mTOR pathway with a specific PI3Kαinhibitor(BYL719)or an mTOR inhibitor(everolimus)reduced the protein levels of Cyclin D1 and CDK4,and restored the sensitivity to palbociclib.The tumor samples expressed significantly higher levels of Cyclin D1,CDK4,p-AKT and p-4E-BP1 after progression on palbociclib treatment.In conclusion,our findings suggest that overexpressed Cyclin D1 and CDK4 proteins lead to the resistance to CDK4/6 inhibitor and PI3K/mTOR inhibitors are able to restore the sensitivity to CDK4/6 inhibitors,which provides the biomarker and rationale for the combinational use of CDK4/6 inhibitors and PI3K/mTOR inhibitors after CDK4/6 inhibitor resistance in breast cancer. | Zijie Cai Jingru Wang Yudong Li Qianfeng Shi Liang Jin Shunying Li Mengdi Zhu Qi Wang Lok Lam Wong Wang Yang Hongna Lai Chang Gong Yandan Yao Yujie Liu Jun Zhang Herui Yao Qiang Liu | 2023 | Science China(Life Sciences)2023，66，1： | 4 |
| 3 | A Positive Feedback Loop between Mesenchymal-like Cancer Cells and Macrophages Is Essential to Breast Cancer Metastasis显示文摘 | Shicheng Su Qiang Liu Jingqi Chen Jianing Chen Fei Chen Chonghua He Di Huang Wei Wu Ling Lin Wei Huang Jin Zhang Xiuying Cui Fang Zheng Haiyan Li Herui Yao Fengxi Su Erwei Song | 2014 | Cancer Cell2014，，5： | 3 |
| 4 | Overexpression of PITPNM3 promotes hepatocellular carcinoma cell metastasis显示文摘A previous study indicated that C–C chemokine(C–C motif)ligand 18(CCL18)is capable of inducing tumor cell invasion and metastasis by interacting with receptor membrane-associated phosphatidylinositol transfer protein 3(PITPNM3)in breast cancer cells.The present study aims to investigate the correlation between the PITPNM3 expression and metastasis in hepatocellular carcinoma(HCC).Real-time quantitative polymerase chain reaction and Western blot were performed to detect the expression pattern of PITPNM3 in patient samples and HCC cell lines.Wound-healing and transwell chamber assays were performed to assess the migration and invasiveness of HCC cells,and the activation of the signaling protein downstream of PITPNM3 was also detected by Western blot and immunofluorescence.The results revealed that PITPNM3 was upregulated in HCC tissue compared to matched normal liver tissue.Silencing the expression of PITPNM3 by specific siRNAs markedly attenuated the invasive and metastatic abilities of HCC cells,whereas the upregulation of PITPNM3 significantly increased HCC cell mobility.Furthermore,inhibiting the expression of PITPNM3 suppressed the activation of Pyk2,FAK,and Src,while overexpression of PITPNM3enhanced the phosphorylation of FAK and Src in HCC cells.Besides,suppression of Pyk2 can also impair the clustering of integrin.These results imply that PITPNM3 is a vital determinant of HCC migration and invasion. | Chonghua He Shicheng Su Fei Chen Di Huang Fang Zheng Wei Huang Jianing Chen Xiuying Cui Qiang Liu Erwei Song Herui Yao Yujie Liu | 2014 | Chinese Science Bulletin2014，59，12： | 3 |
| 5 | Divisional and hierarchical innervations of G. gecko's toes to motion and reception显示文摘As a member of robot families, climbing robots have become one of the research hot-spots in the robotic field recently and Gekko gecko (G. gecko) has been broadly seen as an ideal model for climbing robot development. But for gecko-mimic robots, one of the key problems is how to design the robot's foot. In this paper, (1) high-speed camera recording and electrophysiological method are used to observe motion patterns of G. gecko's foot when it climbs on different oriented surfaces; (2) nerve innervations of gecko's toes to motion and reception are studied. It is found that the five toes of the G. gecko can be divided into two motion and reception divisions, and also its motion and reception are modulated and controlled hierarchically. The results provide important information and exclusive ideas for the foot design and control algorithm of gecko-mimic robots. | GUO Ce CAI Lei XIE HeRui WANG ZhouYi DAI ZhenDong SUN JiuRong | 2009 | Chinese Science Bulletin2009，54，16： | 3 |
| 6 | Current management of chemotherapy-induced neutropenia in adults:key points and new challenges显示文摘Chemotherapy-induced neutropenia(CIN)is a potentially fatal and common complication in myelosuppressive chemotherapy.The timing and grade of CIN may play prognostic and predictive roles in cancer therapy.CIN is associated with older age,poor functional and nutritional status,the presence of significant comorbidities,the type of cancer,previous chemotherapy cycles,the stage of the disease,specific chemotherapy regimens,and combined therapies.There are many key points and new challenges in the management of CIN in adults including:(1)Genetic risk factors to evaluate the patient’s risk for CIN remain unclear.However,these risk factors urgently need to be identified.(2)Febrile neutropenia(FN)remains one of the most common reasons for oncological emergency.No consensus nomogram for FN risk assessment has been established.(3)Different assessment tools[e.g.,Multinational Association for Supportive Care in Cancer(MASCC),the Clinical Index of Stable Febrile Neutropenia(CISNE)score model,and other tools]have been suggested to help stratify the risk of complications in patients with FN.However,current tools have limitations.The CISNE score model is useful to support decision-making,especially for patients with stable FN.(4)There are still some challenges,including the benefits of granulocyte colony stimulating factor treatment and the optimal antibiotic regimen in emergency management of FN.In view of the current reports,our group discusses the key points,new challenges,and management of CIN. | Committee of Neoplastic Supportive-Care(CONS),China Anti-Cancer Association Committee of Clinical Chemotherapy,China Anti-Cancer Association Yi Ba Yuankai Shi Wenqi Jiang Jifeng Feng Ying Cheng Li Xiao Qingyuan Zhang Wensheng Qiu Binghe Xu Ruihua Xu Bo Shen Zhiguo Luo Xiaodong Xie Jianhua Chang Mengzhao Wang Yufu Li Yuerong Shuang Zuoxing Niu Bo Liu Jun Zhang Li Zhang Herui Yao Conghua Xie Huiqiang Huang Wangjun Liao Gongyan Chen Xiaotian Zhang Hanxiang An Yanhong Deng Ping Gong Jianping Xiong Qinghua Yao Xin An Cheng Chen Yanxia Shi Jialei Wang Xiaohua Wang Zhiqiang Wang Puyuan Xing Sheng Yang Chenfei Zhou | 2020 | Cancer Biology & Medicine2020，17，4： | 2 |
| 7 | One pot synthesis, crystal structures and properties of two new MOFs with imidazole-containing tripodal ligand显示文摘Two new different Cu(Ⅱ) MOFs with the same 1,3,5-tris(1-imidazolyl) benzene(tib) ligand {[Cu(tib)2]·(H2O)2·Br2}n(1) and {[Cu2(tib)·Br·Cl]·2Br}n(2) were obtained by one pot synthesized of tib with CuBr in the presences of HCl and water. X-ray single crystal diffraction analyses indicate that both complexes 1 and 2 have two dimensional frameworks containing different building blocks. Each Cu(Ⅱ) atom in complex 1 is coordinated by four N atoms from different tib ligands. However, there are two different cryptographic Cu(Ⅱ) atoms in complex 2, one is four coordinated by two bromine atoms and two N atoms from different tib ligands, the other is six coordinated by two chloride atoms and four N atoms from different tib ligands. The thermal gravimetric analysis of complexes 1 and 2 are depicted in the paper. | TANG YunZhi YU YinMei XIONG JianBo YAO Qiong TAN YuHui GAO JiXing WEN HeRui | 2014 | Science China Chemistry2014，57，11： | 2 |
| 8 | Let-7 regulates self renewal and tumorigenicity of breast cancer cells显示文摘 | Fengyan Y Herui Y Pengcheng Zhu | 2007 | Cell2007，131，： | 1 |
| 9 | Upregulation of GLT25D1 in Hepatic Stellate Cells Promotes Liver Fibrosis via the TGF-β1/SMAD3 Pathway In Vivo and In vitro显示文摘Background and Aims:Collagenβ(1-O)galactosyltransferase 25 domain 1(GLT25D1)is associated with collagen production and glycosylation,and its knockout in mice results in embryonic death.However,its role in liver fibrosis remains elusive,particularly in hepatic stellate cells(HSCs),the primary collagen-producing cells associated with liver fibrogenesis.Herein,we aimed to elucidate the role of GLT25D1 in HSCs.Methods:Bile duct ligation(BDL)-induced mouse liver fibrosis models,primary mouse HSCs(mHSCs),and transforming growth factor beta 1(TGF-β1)-stimulated LX-2 human hepatic stellate cells were used in in vivo and in vitro studies.Stable LX-2 cell lines with either GLT25D1 overexpression or knockdown were established using lentiviral transfection.RNA-seq was performed to investigate the genomic differences.HPLCMS/MS were used to identify glycosylation sites.Scanning electronic microscopy(SEM)and second-harmonic generation/two-photon excited fluorescence(SHG/TPEF)were used to image collagen fibril morphology.Results:GLT25D1 expression was upregulated in nonparenchymal cells in human cirrhotic liver tissues.Meanwhile,its knockdown attenuated collagen deposition in BDL-induced mouse liver fibrosis and inhibited mHSC activation.GLT25D1 was overexpressed in activated versus quiescence LX-2 cells and regulated in vitro LX-2 cell activation,including proliferation,contraction,and migration.GLT25D1 also significantly increased liver fibrogenic gene and protein expression.GLT25D1 upregulation promoted HSC activation and enhanced collagen expression through the TGF-β1/SMAD signaling pathway.Mass spectrometry showed that GLT25D1 regulated the glycosylation of collagen in HSCs,affecting the diameter of collagen fibers.Conclusions:Collectively,the upregulation of GLT25D1 in HSCs promoted the progression of liver fibrosis by affecting HSCs activation and collagen stability. | Shiwei Wang Lingling He Fan Xiao Meixin Gao Herui Wei Junru Yang Yang Shu Fuyang Zhang Xiaohui Ye Ping Li Xiaohua Hao Xingang Zhou Hongshan Wei | 2023 | Journal of Clinical and Translational Hepatology2023，11，1： | 1 |
| 10 | Synthesis process and luminescence properties of Tm^3+ in AWO4 (A=Ca, Sr, Ba) blue phosphors显示文摘 | Jinsheng Liao Bao Qiu Herui Wen et ai | 2009 | Journal of Alloys and Compounds2009，487，： | 1 |
| 11 | Let-7 regulates self renewal and tumorigenicity of breast cancer cells显示文摘 | Herui Yao Pengcheng Zhu | 2007 | Cell2007，131，6： | 1 |
| 12 | Let-7 regulates self renewal and tumorigenicity of breast cancer cells 显示文摘 | Fengyan Yu Herui Yao Pengcheng Zhu Xiaoqin Zhang Qiuhui Pan Chang Gong Yijun Huang Xiaoqu Hu Fengxi Su Judy Lieberman and Erwei Song | 2007 | Cell 20072007，，： | 1 |
| 13 | Photoluminescence green in microspheres of CaWO 4 :Tb 3+ processed in conventional hydrothermal显示文摘 | Jinsheng Liao Bao Qiu Herui Wen Weixiong You | 2009 | Optical Materials2009，，10： | 1 |
| 14 | Synthesis and optimum luminescence of monodispersed spheres for BaWO 4 -based green phosphors with doping of Tb 3+显示文摘 | Jinsheng Liao Bao Qiu Herui Wen Weixiong You Youjun Xiao | 2009 | Journal of Luminescence2009，，5： | 1 |
| 15 | Simulation of pedestrian flow on square lattice based on cellular au- tomata model显示文摘 | Hao Yue Herui Hao Xiaoming Chen | 2007 | Physica A: Statistical Mechanics and its Applications2007，384，2： | 1 |
| 16 | CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3显示文摘 | Jingqi Chen Yandan Yao Chang Gong Fengyan Yu Shicheng Su Jianing Chen Bodu Liu Hui Deng Fengsong Wang Ling Lin Herui Yao Fengxi Su Karen S. Anderson Qiang Liu Mark E. Ewen Xuebiao Yao Erwei Song | 2011 | Cancer Cell2011，，4： | 1 |
| 17 | Dopant concentration dependence of structure, optical, and magnetic properties of ZnO:Fe thin films显示文摘 | Ruijin Hong Herui Wen Caiming Liu Jinglin Chen Jinsheng Liao | 2010 | Journal of Crystal Growth2010，，1： | 1 |
| 18 | Synthesis process and luminescence properties of Tm 3+ in AWO 4 (A显示文摘 | Jinsheng Liao Bao Qiu Herui Wen Jinglin Chen Weixiong You Liangbin Liu | 2009 | Journal of Alloys and Compounds2009，，1： | 1 |
| 19 | IgG subclass distribution of antibody responses to protein and polyscharide mycobacterial antigen in leprosy and tuberculosis patients 显示文摘 | Souss AO Heruy S Maroja FM | 1998 | Clin Ekp Immunol1998，111，1： | 1 |
| 20 | 显示文摘 | Liao Jinsheng Qiu Bao Wen Herui | 2009 | Materials Research Bulletin2009，44，9： | 1 |
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