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Oncogenic ADAM28 induces gemcitabine resistance and predicts a poor prognosis in pancreatic cancer

World Journal of Gastroenterology 2019年第37期25卷 5590-5603页

作者： Li Wei Jing-Yun Wen Jie chen Xiao-Kun Ma Dong-Hao Wu zhan-hong chen Jiang-Long Huang Department of Medical Oncology The Third Affiliated Hospital of Sun Yat-Sen UniversityGuangzhou 510630Guangdong ProvinceChina Department of Gastrointestinal Surgery The Third Affiliated Hospital of Sun Yat-Sen UniversityGuangzhou 510630Guangdong ProvinceChina

BACKGROUND Pancreatic cancer is a major cause of cancer-related death,with a 5-year overall survival rate being below 5%.The main causes of poor prognosis in pancreatic cancer include easy metastasis,high recurrence rate,and robust drug *** is a first-line drug for patients with unresectable pancreatic ***,due to drug resistance,the clinical effect is not ***28 is reported as a tumor promoter in some cancers,but its role in pancreatic cancer and gemcitabine chemoresistance in pancreatic cancer has not been *** To identify if ADAM28 can act as an important target to reverse the gemcitabine drug resistance in pancreatic *** RNA-sequence analysis was applied to explore the potential targets involved in the gemcitabine of pancreatic ***1990 pancreatic cancer cells were treated with an increased dose of gemcitabine,and the mRNA levels of ADAM28 were evaluated by *** protein and mRNA levels of ADAM28 were confirmed in the gemcitabine resistant and parallel SW1990 *** ADAM28 expression was also assessed in TCGA and GEO databases,and the results were confirmed in the collected tumor and adjacent normal *** overall survival(OS)rate and relapse-free survival(RFS)rate of pancreatic cancer patients with high ADAM28 level and low ADAM28 level in TCGA were evaluated with Kaplan-Meier ***,the OS rate was calculated in pancreatic cancer patients with high tumor mutation burden(TMB)and low ***-8 assay was used to examine the effect of ADAM28 on the viability of SW1990 *** ADAM28 and its co-expressed genes were analyzed in the cBioPortal for cancer genomics and subjected to GSEA pathway *** correlations of ADAM28 with GSTP1,ABCC1,GSTM4,and BCL2 were analyzed based on TCGA data on pancreatic *** RNA-sequence analysis identified that ADAM28 was overexpressed in gemcitabine-resistant cells,and gemcitabine treatment could induce the expression of ADAM

关键词： ADAM28 Drug resistance Overexpression Poor prognosis Drug metabolism Gemcitabine

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Theoretical Comparison of Oxygen Adsorption on Cu（100） Surface

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Chinese Journal of Chemical Physics 2006年第1期19卷 54-58页

作者： Wen-kai chen Chun-hai Lu zhan-hong chen Yi Li Jun-qian Li Department of Chemistry Fuzhou University Fuzhou 350002 China China Academy of Engineering Physics Mianyang 521900 China State Key Laboratory of Structural Chemistry Fuzhou 3500021 China

The interaction of atomic oxygen with the clean Cu（100） surface has been studied by means of cluster and periodic slab models density functional theory in the present paper. The Cu（4,9,4） cluster and a three-layer slab with c（2×2） structure are used to model the perfect Cn（100） surface. Three possible adsorption sites, top, bridge and hollow site, were considered in the calculations. The predicted results show that the hollow site is the prefer site for atomic oxygen adsorbed on Cu（100） surface energetically. This is in good agreement with the experiment. The calculated binding energies are respective 2.014, 3.154 and 3.942 eV for top, bridge and hollow sites at mPW1PW91/LanL2dz level for the cluster model. The geometry of Cu（100） surface has also been optimized theoretically with various density functional rnethods and the results show that the prediction from the B3PW91/LanL2dz and mPWlPW91/LanL2dz reproduce the experimental observation. The frontier molecular orbitals and partial density of states analysis show that the electron transfer from the d orbital of substrate to the p orbital of the surface oxygen atom.

关键词： Oxygen Density functional theory Cu(100) surface Adsorption

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Lymphocyte-to-monocyte ratio predicts survival of patients with hepatocellular carcinoma after curative resection

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World Journal of Gastroenterology 2015年第38期21卷 10898-10906页

作者： Ze-Xiao Lin Dan-Yun Ruan Yang Li Dong-Hao Wu Xiao-Kun Ma Jie chen zhan-hong chen Xing Li Tian-Tian Wang Qu Lin Jing-Yun Wen Xiang-Yuan Wu Department of Medical Oncology The Third Affiliated Hospital of Sun Yat-sen University Department of Liver Surgery The Third Affiliated Hospital of Sun Yat-sen University

AIM: To investigate the prognostic value of preoperative lymphocyte-to-monocyte ratio(LMR) in patients with hepatocellular carcinoma(HCC) undergoing curative ***: Clinicopathological data of 210 hepatitis B virus(HBV)-associated HCC patients who were treated by radical hepatic resection between 2003 and 2010 were retrospectively analyzed. None of the patients received any preoperative anticancer therapyor intraoperative radiofrequency ablation. The diagnosis was confirmed by pathological examination after surgery. Absolute peripheral blood lymphocyte and monocyte counts were derived from serum complete blood cell count before surgery,and LMR was calculated by dividing lymphocyte count by monocyte count. The best cutoff was determined by receiver operating characteristics(ROC) curve analysis. Correlations between LMR levels and clinicopathological features were assessed using the χ2 test. Survival outcomes were estimated using the Kaplan-Meier method and compared by the log-rank test. Univariate and multivariate analyses were performed to evaluate the prognostic impact of LMR and other clinicopathological factors on overall survival(OS) and recurrence-free survival(RFS),using the Cox proportional hazards ***: The optimal cutoff value of LMR for survival analysis was 3.23,which resulted in the most appropriate sensitivity of 55.3% and specificity of 74.7%,with the area under the curve(AUC) of 0.66(95%CI: 0.593-0.725). All patients were dichotomized into either a low(≤ 3.23) LMR group(n = 66) or a high(> 3.23) LMR group(n = 144). A low preoperative LMR level was significantly correlated with the presence of cirrhosis,elevated levels of total bilirubin and larger tumor size. Patients with a low LMR level had significantly reduced 5-year OS(61.9% vs 83.2%,P < 0.001) and RFS(27.8% vs 47.6%,P = 0.009) compared to those with a high LMR level. Multivariate analyses indicated that a lower LMR level was a significantly independent predictor of inferio

关键词： Hepatocellular carcinoma Liver resection Lymphocyt

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VDR–SOX2 signaling promotes colorectal cancer stemness and malignancy in an acidic microenvironment

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Signal Transduction and Targeted Therapy 2020年第1期5卷 852-864页

作者： Pei-Shan Hu Ting Li Jin-Fei Lin Miao-Zhen Qiu De-Shen Wang Ze-Xian Liu zhan-hong chen Lu-Ping Yang Xiao-Long zhang Qi Zhao Yan-Xing chen Yun-Xin Lu Qi-Nian Wu Heng-Ying Pu Zhao-Lei Zeng Dan Xie Huai-Qiang Ju Hui-Yan Luo Rui-Hua Xu Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer Center510060 GuangzhouPeople’s Republic of China Precision Diagnosis and Treatment for Gastrointestinal Cancer Chinese Academy of Medical Sciences510060 GuangzhouPeople’s Republic of China Department of Medical Oncology and Guangdong Key Laboratory of Liver Disease the Third Affiliated Hospital of Sun Yat-sen University510060 GuangzhouPeople’s Republic of China

The acidic tumor microenvironment provides an energy source driving malignant tumor *** of cells to an acidic environment leads to the emergence of cancer stem *** expression of the vitamin D receptor(VDR)is closely related to the initiation and development of colorectal carcinoma(CRC),but its regulatory mechanism in CRC stem cells is still *** study revealed that acidosis reduced VDR expression by downregulating peroxisome proliferator-activated receptor delta(PPARD)*** of VDR effectively suppressed the stemness and oxaliplatin resistance of cells in *** nuclear export signal in VDR was sensitive to acidosis,and VDR was exported from the *** immunoprecipitation(ChIP)and assay for transposase-accessible chromatin with high-throughput sequencing(ATAC-seq)analyses showed that VDR transcriptionally repressed SRY-box 2(SOX2)by binding to the vitamin D response elements in the promoter of SOX2,impairing tumor growth and drug *** demonstrated that a change in the acidic microenvironment combined with overexpression of VDR substantially restricted the occurrence and development of CRC in *** findings reveal a new mechanism by which acidosis could affect the stemness of CRC cells by regulating the expression of SOX2 and show that abnormal VDR expression leads to ineffective activation of vitamin D signaling,resulting in a lack of efficacy of vitamin D in antineoplastic process.

关键词： SOX2 vitamin colorectal

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网络外部性下我国企业技术引进策略

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上海交通大学学报 2008年第11期42卷 1818-1822页

作者：刘展陈宏民上海交通大学安泰经济与管理学院上海200052

利用Hotelling模型所构建的多维产品差异化模型,深入研究了在具有产品网络外部性特征的行业中,我国政府和企业的优化技术引进策略,指出当国际可选择技术与我国自主研发技术质量差距较大时,技术引进国政府应鼓励本国企业引进尽可能高质... 详细信息

利用Hotelling模型所构建的多维产品差异化模型,深入研究了在具有产品网络外部性特征的行业中,我国政府和企业的优化技术引进策略,指出当国际可选择技术与我国自主研发技术质量差距较大时,技术引进国政府应鼓励本国企业引进尽可能高质量的技术;当国际可选择技术与我国自主研发技术质量差距较小时,我国政府应限制本国的技术引进活动;在推动本国企业技术引进活动时,技术引进国应权衡比较引进技术与原有技术的质量差距、技术之间兼容性、技术许可收费比例、技术引进的技术溢出强度等因素,并强调技术企业拥有新技术的知识产权.在此基础上,提出相应的政策建议.

关键词：技术引进网络外部性自主创新

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AZD1775 synergizes with SLC7A11 inhibition to promote ferroptosis

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Science China Life Sciences 2025年第1期68卷 204-218页

作者： chen Xiong hong Ling Yingdan Huang Hanzhi Dong Bangxiang Xie Qian Hao Xiang Zhou Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences Fudan University Department of Oncology Shanghai Medical CollegeFudan University Department of Breast Surgery Fudan University Shanghai Cancer CenterFudan University Department of Oncology First Affiliated Hospital of Nanchang University Beijing Institute of Hepatology Beijing Youan HospitalCapital Medical University Beijing Engineering Research Center for Precision Medicine and Transformation of Hepatitis and Liver Cancer Key Laboratory of Breast Cancer in Shanghai Fudan University Shanghai Cancer CenterFudan University Shanghai Key Laboratory of Medical Epigenetics International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology)Institutes of Biomedical SciencesFudan University

Tumor suppressor p53-mediated cell cycle arrest and DNA damage repair may exert cytoprotective effects against cancer therapies, including WEE1 inhibition. Considering that p53 activation can also lead to multiple types of cell death, the role of this tumor suppressor in WEE1 inhibitor-based therapies remains disputed. In this study, we reported that nucleolar stress-mediated p53 activation enhanced the WEE1 inhibitor AZD1775-induced ferroptosis to suppress lung cancer growth. Our findings showed that AZD1775 promoted ferroptosis by blocking cystine uptake, an action similar to that of Erastin. Meanwhile, inhibition of WEE1 by the WEE1 inhibitors or si RNAs induced compensatory upregulation of SLC7A11, which conferred resistance to ferroptosis. Mechanistically, AZD1775 prevented the enrichment of H3K9me3, a histone marker of transcriptional repression, on the SLC7A11 promoter by repressing the expression of the histone methyltransferase SETDB1, thereby enhancing NRF2-mediated SLC7A11 transcription. This finding was also validated using the H3K9me3 inhibitor BRD4770. Remarkably, we found that the nucleolar stress-inducing agent Actinomycin D(Act. D) inhibited SLC7A11 expression by activating p53, thus augmenting AZD1775-induced ferroptosis. Moreover, the combination of AZD1775 and Act. D synergistically suppressed wild-type p53-harboring lung cancer cell growth both in vitro and in vivo. Altogether, our study demonstrates that AZD1775 promotes ferroptosis by targeting cystine uptake but also mediates the adaptive activation of SLC7A11 through the WEE1-SETDB1 cascade and NRF2-induced transcription, and inhibition of SLC7A11 by Act. D boosts the anti-tumor efficacy of AZD1775 by enhancing ferroptosis in cancers with wild-type p53.

关键词： p53 NRF2 SLC7A11 WEE1 AZD1775 ferroptosis nucleolar stress

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Advances in therapies using mesenchymal stem cells and their exosomes for treatment of peripheral nerve injury:state of the art and future perspectives

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Neural Regeneration Research 2025年第11期20卷 3151-3171页

作者： Fatima Aldali Chunchu Deng Mingbo Nie hong chen Department of Rehabilitation Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina Department of Orthopedics Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina

“Peripheral nerve injury”refers to damage or trauma affecting nerves outside the brain and spinal *** nerve injury results in movements or sensation impairments,and represents a serious public health *** severed peripheral nerves have been effectively joined and various therapies have been offered,recovery of sensory or motor functions remains limited,and efficacious therapies for complete repair of a nerve injury remain *** emerging field of mesenchymal stem cells and their exosome-based therapies hold promise for enhancing nerve regeneration and *** stem cells,as large living cells responsive to the environment,secrete various factors and *** latter are nano-sized extracellular vesicles containing bioactive molecules such as proteins,microRNA,and messenger RNA derived from parent mesenchymal stem *** have pivotal roles in cell-to-cell communication and nervous tissue function,offering solutions to changes associated with cell-based *** ongoing investigations,mesenchymal stem cells and mesenchymal stem cell-derived exosome-based therapies are in the exploratory stage.A comprehensive review of the latest preclinical experiments and clinical trials is essential for deep understanding of therapeutic strategies and for facilitating clinical *** review initially explores current investigations of mesenchymal stem cells and mesenchymal stem cell-derived exosomes in peripheral nerve injury,exploring the underlying ***,it provides an overview of the current status of mesenchymal stem cell and exosomebased therapies in clinical trials,followed by a comparative analysis of therapies utilizing mesenchymal stem cells and ***,the review addresses the limitations and challenges associated with use of mesenchymal stem cell-derived exosomes,offering potential solutions and guiding future directions.

关键词： clinical trials exosome extracellular vesicles mesenchymal stem cells nerve regeneration peripheral nerve injury pre-clinical experiments

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双视系统的室内三维场景重建研究

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计算机科学 2020年第S2期47卷 175-177页

作者：陈颖赵来旺詹洪陈丁尧南京大学金陵学院南京210089

在早期三维场景重建中,受硬件条件的限制,无法很好地对场景进行三维重建。随着硬件的更新迭代,目前可利用结构光和双视系统进行更加高效的三维场景重建。以ZED双目相机和捷宝AD-10电动云台构建硬件平台,通过双目相机获得场景的点云信息... 详细信息

在早期三维场景重建中,受硬件条件的限制,无法很好地对场景进行三维重建。随着硬件的更新迭代,目前可利用结构光和双视系统进行更加高效的三维场景重建。以ZED双目相机和捷宝AD-10电动云台构建硬件平台,通过双目相机获得场景的点云信息,基于全局SBGM(Semi-Global Block Matching)算法的立体匹配和RGB-D图(Red Green Blue Depth Map)的生成来进行单一场景点云重建,并通过ORB特征匹配和ICP(Iterative Closest Point)点云配准融合,实现对室内场景的全景三维重建。实验对比了双目立体视觉的场景重建在过远/过近目标、低纹理特征目标、玻璃等材质目标上的优势,同时在点云的三维场景重建中,提出通过稀疏化来优化点云信息,对比单一采集与多次采集的重建效果。经过实验,该系统在折中采用次数的前提下,可以兼顾场景重建细节与显示效果,并对不同场景目标的三维重建具有实际的工程借鉴意义和应用价值。

关键词：三维场景重建双目视觉全景场景重建 PCL ICP

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Overexpression of low-density lipoprotein receptor prevents neurotoxic polarization of astrocytes via inhibiting NLRP3 inflammasome activation in experimental ischemic stroke

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Neural Regeneration Research 2025年第2期20卷 491-502页

作者： Shuai Feng Juanji Li Tingting Liu Shiqi Huang Xiangliang chen Shen Liu Junshan Zhou hongdong Zhao Ye hong Department of Neurology Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Neurology Nanjing Jinling HospitalAffiliated Hospital of Medical SchoolNanjing UniversityNanjingJiangsu ProvinceChina

Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion ***-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit NLR family pyrin domain containing protein 3(NLRP3)inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s ***,little is known about the effects of low-density lipoprotein receptor on astrocytic activation in ischemic *** address this issue in the present study,we examined the mechanisms by which low-density lipoprotein receptor regulates astrocytic polarization in ischemic stroke ***,we examined low-density lipoprotein receptor expression in astrocytes via immunofluorescence staining and western blotting *** observed significant downregulation of low-density lipoprotein receptor following middle cerebral artery occlusion reperfusion and oxygen-glucose deprivation/***,we induced the astrocyte-specific overexpression of low-density lipoprotein receptor using astrocyte-specific adeno-associated ***-density lipoprotein receptor overexpression in astrocytes improved neurological outcomes in middle cerebral artery occlusion mice and reversed neurotoxic astrocytes to create a neuroprotective ***,we found that the overexpression of low-density lipoprotein receptor inhibited NLRP3 inflammasome activation in oxygen-glucose deprivation/reoxygenation injured astrocytes and that the addition of nigericin,an NLRP3 agonist,restored the neurotoxic astrocyte *** findings suggest that low-density lipoprotein receptor could inhibit the NLRP3-meidiated neurotoxic polarization of astrocytes and that increasing low-density lipoprotein receptor in astrocytes might represent a novel strategy for treating cerebral ischemic stroke.

关键词： inflammation ischemia/reperfusion injury ischemic stroke low-density lipoprotein receptor neuroprotective astrocytes neurotoxic astrocytes NLRP3 inflammasome polarization

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Stable copper boron–imidazolate cage as Cu-riched enzyme for highly efficient electrocatalytic CO2 reduction to ethylene

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Science China Chemistry 2025年

作者： Jun-Qiang chen Qiao-hong Li Qin-Long hong Ping Shao Hai-Xia zhang Jian zhang State Key Laboratory of Structural Chemistry Fujian Institute of Research on the Structure of Matter Chinese Academy of Sciences

Single-atom catalyst has garnered widespread attention to mimic mature enzymes due to its well-defined atomic structure and coordination environments. However, since the carbon–carbon（C–C） coupling reactions require synergistic catalysis of multiple sites, single-atom catalysts suffer from insufficient active sites and unclear reaction mechanisms. Controlling the reaction intermediates in a precisely targeted pocket through careful metal–organic cage design is therefore crucial. Here, we prepare a tetrahedral [Cu6L4]-type boron–imidazolate cage integrating highly active Cu sites and optimized cavity, which exhibits enzyme like specific catalytic performance in electrochemical CO2reduction reaction（CO2RR） to enhance the selectivity of *** analyses and computational calculations suggest that the single Cu site together with neighboring boron–imidazolate ligands provides suitably synergistic effects that enable the energetically favorable formation of an *COCHO intermediate, a key step determining selectivity. As a result, the [Cu6L4]-type cage of BIC-145 achieves a Faradaic efficiency of 28% for C2H4maintaining an average current density of -3.54 mA cm-2over a 5-hour electrolysis period. This work represents the first example for studying single-metal site catalysts with ultra-low coordination numbers through the rational design of metal–organic cages.

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