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Alpha5 nicotine acetylcholine receptor subunit promotes intrahepatic cholangiocarcinoma metastasis

Signal Transduction and Targeted Therapy 2024年第4期9卷 1690-1705页

作者： Yan Fu Keyu Shen Hao Wang Shun Wang Xufeng Wang Le Zhu Yan Zheng Tiantian Zou Hongfei Ci qiongzhu dong Lun-Xiu Qin Hepatobiliary Surgery Department of General SurgeryHuashan Hospital&Cancer Metastasis InstituteFudan University200040 ShanghaiChina Center of Interventional Radiology and Vascular Surgery Department of RadiologyZhongda HospitalMedical SchoolSoutheast University87 Dingjiaqiao Road210009 NanjingChina institutes of Biomedical Sciences Fudan University200032 ShanghaiChina Key Laboratory of Whole-period Monitoring and Precise Intervention of Digestive Cancer Shanghai Municipal Health CommissionMinhang HospitalFudan UniversityShanghaiChina

Neurotransmitter-initiated signaling pathway were reported to play an important role in regulating the malignant phenotype of tumor *** cells could exhibit a"neural addiction"property and build up local nerve networks to achieve an enhanced neurotransmitter-initiated signaling through nerve growth factor-mediated *** the dysregulated nervous systems might represent a novel strategy for cancer ***,whether intrahepatic cholangiocarcinoma(ICC)could build its own nerve networks and the role of neurotransmitters in the progression ICC remains largely *** staining and Enzyme-linked immunosorbent assay suggested that IcC cells and the infiltrated nerves could generate a tumor microenvironment rich in acetylcholine that promotes IcC metastasis by inducing epithelial-mesenchymal transition(EMT).Acetylcholine promoted iCC metastasis through interacting with its receptor,alpha 5 nicotine acetylcholine receptor subunits(CHRNA5).Furthermore,acetylcholine/CHRNA5 axis activated GSK3β/β-catenin signaling pathway partially through the influx of Ca^(2+)-mediated activation of Ca/calmodulin-dependent protein kinases(CAMKll).In addition,acetylcholine signaling activation also expanded nerve infiltration through increasing the expression of Brain-Derived Neurotrophic Factor(BDNF),which formed a feedforward acetylcholine-BDNF axis to promote ICC ***93,a small-molecule inhibitor of CAMKIll,significantly inhibited the migration and enhanced the sensitivity to gemcitabine of ICC *** all,Acetylcholine/CHRNA5 axis increased the expression ofβ-catenin to promote the metastasis and resistance to gemcitabine of ICC via CAMKIl/GSK3βsignaling,and the CAMKIl inhibitor KN93 may be an effective therapeutic strategy for combating ICC metastasis.

关键词： GSK3β metastasis Alpha

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A Prognostic Nomogram for Hepatocellular Carcinoma Based on Wound Healing and Immune Checkpoint Genes

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Journal of Clinical and Translational Hepatology 2022年第5期10卷 891-900页

作者： Beiyuan Hu Xiaotian Shen Wei Qin Lan Zhang Tiantian Zou qiongzhu dong Lun-Xiu Qin Department of General Surgery Huashan Hospital&Cancer Metastasis InstituteInstitutes of Biomedical SciencesFudan UniversityShanghaiChina

Background and Aims:Wound healing and tumor progression share some common biological features;however,how variations in wound healing patterns affect hepatocellular carcinoma(HCC)prognosis remains ***:We analyzed the wound healing patterns of 594 HCC samples from The Cancer Genome Atlas(TCGA)and the International Cancer Genome Consortium(ICGC)and correlated them with immune infiltration and the expression levels of immune checkpoint genes.A risk score,which we named the“***”score,was established via stepwise Cox *** constructed a nomogram based on age,sex,TNM stage,and *** score and explored its predictive value for HCC ***-four clinical patients were enrolled in this study,and all were from Huashan Hospital of Fudan University between 2015 and 2017 to serve as an independent validation ***:We identified two distinct wound healing patterns in *** biological processes of healing cluster 1(C1)are related to metabolism,while those of healing cluster 2(C2)are related to the inflammatory response and immune cell accumulation.A total of 565 wound healing-related genes(based on Gene Ontology)and 25 immune checkpoint genes were *** analyzing differentially expressed genes and implementing a stepwise Cox estimation analysis,six genes with p values less than 0.02 in a multivariate Cox estimation were chosen as the“***”gene set(FCER1G,PLAT,ITGA5,CCNB1,CD86 and CD40).The“***”gene set,as an OS risk factor,was further validated in Fudan *** constructed a nomogram to predict the 1-,3-and 5-year overall survival(OS)in the TCGA *** area under curve vales of the receiver characteristic operator curves were 0.82,0.76 and 0.73 in the training group and 0.84,0.76 and 0.72 in the test ***:We established a prognostic nomogram based on the *** gene signature,which includes six wound healing-and immunity-related *** nomogram accurately predicts the OS of HCC

关键词： Hepatocellular carcinoma Bioinformatics Immune checkpoint Wound healing Prognosis

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Rapamycin enhances the anti-tumor activity of cabozantinib in cMet inhibitor-resistant hepatocellular carcinoma

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Frontiers of Medicine 2022年第3期16卷 467-482页

作者： Chao Gao Shenghao Wang Weiqing Shao Yu Zhang Lu Lu Huliang Jia Kejin Zhu Jinhong Chen qiongzhu dong Ming Lu Wenwei Zhu Lunxiu Qin Department of General Surgery Huashan HospitalCancer Metastasis InstituteFudan UniversityShanghai 200040China Kanion Research Institute Lianyungang 222002China Institutes of Biomedical Sciences Fudan UniversityShanghai 200040China

Cabozantinib,mainly targeting cMet and vascular endothelial growth factor receptor 2,is the second-line treatment for patients with advanced hepatocellular carcinoma(HCC).However,the lower response rate and resistance limit its enduring clinical *** this study,we found that cMet-low HCC cells showed primary resistance to cMet inhibitors,and the combination of cabozantinib and mammalian target of rapamycin(mTOR)inhibitor,rapamycin,exhibited a synergistic inhibitory effect on the in vitro cell proliferation and in vivo tumor growth of these ***,the combination of rapamycin with cabozantinib resulted in the remarkable inhibition of AKT,extracellular signal-regulated protein kinases,mTOR,and common downstream signal molecules of receptor tyrosine kinases;decreased cyclin D1 expression;and induced cell cycle ***,rapamycin enhanced the inhibitory effects of cabozantinib on the migration and tubule formation of human umbilical vascular endothelial cells and human growth factor-induced invasion of cMet inhibitor-resistant HCC cells under hypoxia *** effects were further validated in xenograft *** conclusion,our findings uncover a potential combination therapy of cabozantinib and rapamycin to combat cabozantinib-resistant HCC.

关键词： hepatocellular carcinoma cabozantinib primary resistance rapamycin

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A Novel mRNA Signature Related to Immunity to Predict Survival and Immunotherapy Response in Hepatocellular Carcinoma

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Journal of Clinical and Translational Hepatology 2022年第5期10卷 925-938页

作者： Chenhao Zhou Jialei Weng Yuan Gao Chunxiao Liu Xiaoqiang Zhu Qiang Zhou Chia-Wei Li Jialei Sun Manar Atyah Yong Yi Qinghai Ye Yi Shi qiongzhu dong Yingbin Liu Mien-Chie Hung Ning Ren Department of Liver Surgery Liver Cancer InstituteZhongshan Hospitaland Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education)Fudan UniversityShanghaiChina Department of Molecular and Cellular Oncology The University of Texas MD Anderson Cancer CenterHoustonTXUSA Department of Biliary-Pancreatic Surgery Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina School of Biomedical Sciences Li Ka Shing Faculty of MedicineThe University of Hong KongPok Fu LamHong Kong SARChina Biomedical Research Center Zhongshan HospitalFudan UniversityShanghaiChina Institute of Fudan Minhang Academic Health System and Key Laboratory of Whole-period Monitoring and Precise Intervention of Digestive Cancer(SMHC)Minhang Hospital&AHSFudan UniversityShanghaiChina Institutes of Biomedical Sciences Fudan UniversityShanghaiChina Graduate Institute of Biomedical Sciences and Center for Molecular Medicine China Medical UniversityTaichung

Background and Aims:Hepatocellular carcinoma(HCC)is the most common primary liver cancer and the incidence and mortality rates are *** the limited treatments of HCC and promising application of immunotherapy for cancer,we aimed to identify an immune-related prognostic signature that can predict overall survival(OS)rates and immunotherapy response in ***:The initial signature development was conducted using a training dataset from the Cancer Genome Atlas followed by independent internal and external validations from that resource and the Gene Expression Omnibus.A signature based nomogram was generated using multivariate Cox regression *** associations of signature score with tumor immune phenotype and response to immunotherapy were analyzed using single-sample gene set enrichment analysis and tumor immune dysfunction and exclusion algorithm.A cohort from Zhongshan Hospital was employed to verify the pre dictive robustness of the signature regarding prognostic risk and immunotherapy ***:The prognostic signature,IGS_(HCC),consisting of 22 immune-related genes,had independent prognostic ability,with training and validation ***,IGS_(HCC)stratified HCC patients with different outcomes in *** prognostic accuracy of IGS_(HCC)was better than three reported prognostic *** IGS_(HCC)-based nomogram had high accuracy and significant clinical benefits in predicting 3-and 5-year ***_(HCC)reflected distinct immunosuppressive phenotypes in low-and high-score *** with low IGS_(HCC)scores were more likely than those with high scores to benefit from ***:IGS_(HCC)predicted HCC prognosis and response to immunotherapy,and contributed to individualized clinical management.

关键词： Hepatocellular carcinoma Gene signature Immune microenvironment Prognosis Immunotherapy

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The m6A methylation landscape stratifies hepatocellular carcinoma into 3 subtypes with distinct metabolic characteristics

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Cancer Biology & Medicine 2020年第4期17卷 937-952页

作者： Xiaotian Shen Beiyuan Hu Jing Xu Wei Qin Yan Fu Shun Wang qiongzhu dong Lunxiu Qin Department of General Surgery Huashan Hospital&Cancer Metastasis Institute&Institutes of Biomedical SciencesFudan UniversityShanghai 250040China Institutes of Biomedical Sciences Fudan UniversityShanghai 200032China Shanghai Medical College Fudan UniversityShanghai 200040China

Objective:Epigenetic aberration plays an important role in the development and progression of hepatocellular carcinoma(HCC).However,the alteration of RNA N6-methyladenosine(m6A)modifications and its role in HCC progression remain *** therefore aimed to provide evidence using bioinformatics ***:We comprehensively analyzed the m6A regulator modification patterns of 605 HCC samples and correlated them with metabolic alteration *** elucidated 390 gene-based m6A-related signatures and defined an m6Ascore to quantify m6A *** then assessed their values for predicting prognoses and therapeutic responses in HCC ***:We identified 3 distinct m6A modification patterns in HCC,and each pattern had distinct metabolic *** evaluation of m6A modification patterns using m6Ascores could predict the prognoses,tumor stages,and responses to sorafenib treatments of HCC patients.A nomogram based on m6Ascores showed high accuracy in predicting the overall survival of *** area under the receiver operating characteristic curve of predictions of 1,3,and 5-year overall survivals were 0.71,0.69,and 0.70 in the training cohort,and in the test cohort it was 0.74,0.75,and 0.71,respectively.M6Acluster C1,which corresponded to hypoactive mRNA methylation,lower expression of m6A regulators,and a lower m6Ascore,was characterized by metabolic hyperactivity,lower tumor stage,better prognosis,and lower response to sorafenib *** contrast,m6Acluster C3 was distinct in its hyperactive mRNA methylations,higher expression of m6A regulators,and higher m6Ascores,and was characterized by hypoactive metabolism,advanced tumor stage,poorer prognosis,and a better response to *** m6Acluster,C2,was intermediate between C1 and ***:HCCs harbored distinct m6A regulator modification patterns that contributed to the metabolic heterogeneity and diversity of *** of m6A gene signatures and the m6Ascore

关键词： Hepatocellular carcinoma RNA N6-methyladenosine,metabolism,bioinformatics,prognosis

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Development and Validation of a Metabolic Gene-Based Prognostic Signature for Hepatocellular Carcinoma

Development and Validation of a Metabolic Gene-Based Prognos...

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2022CCTB中国肿瘤标志物学术大会暨中国整合肿瘤学...

作者： Jialei Weng Chenhao Zhou Qiang Zhou Wanyong Chen Yirui Yin Manar Atyah qiongzhu dong Yi Shi Ning Ren Zhongshan Hospital Fudan University Department of Molecular and Cellular Oncology The University of Texas MD Anderson Cancer Center Institute of Fudan Minhang Academic Health System Minhang Hospitaland Key Laboratory of Shanghai Municipal Health CommissionFudan University Institutes of Biomedical Sciences Fudan University Biomedical Research Centre Zhongshan HospitalFudan University

Background:Hepatocellular carcinoma(HCC) is a malignant tumor with great variation in prognosis among *** in metabolism influence disease progression and clinical *** objective of this study was to determine the overall survival(OS) risk of HCC patients from a metabolic *** and Methods:The model was constructed using the least absolute shrinkage and selection operator(LASSO) COX regression based on The Cancer Genome Atlas(TCGA,n=342) *** International Cancer Genome Consortium(ICGC,n=232),GSE14520(n=242) datasets,and a clinical cohort(n=64) were then used to assess the prognostic value of the ***:A 10 metabolic gene-based signature was constructed and verified as a robust and independent prognostic classifier in public and real-world validation ***,the signature enabled the identification of HCC molecular subtypes,yielding an AUC value of0.678 [95%CI:0.592-0.763].Besides,the signature was associated with metabolic processes like glycolysis,supported by a clear correlation between the risk score and expression of rate-limiting ***,high-risk tumor was likely to have a high tumor infiltration status of immunosuppressive cells,as well as elevated expression of some immune checkpoint *** final clinical translation,a nomogram integrating the signature and tumor stage was established,and showed improved predictive accuracy of 3-and 5-year OS and brought more net benefit to ***:We developed a prognostic signature based on 10 metabolic genes,which has proven to be an independent and reliable prognostic predictor for HCC and reflects the metabolic and immune characteristics of tumors.

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Exosomal S100A4 derived from highly metastatic hepatocellular carcinoma cells promotes metastasis by activating STAT3

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Signal Transduction and Targeted Therapy 2021年第6期6卷 1895-1906页

作者： Haoting Sun Chaoqun Wang Beiyuan Hu Xiaomei Gao Tiantian Zou Qin Luo Mo Chen Yan Fu Yuanyuan Sheng Kaili Zhang Yan Zheng Xudong Ren Shican Yan Yan Geng Luyu Yang qiongzhu dong Lunxiu Qin Department of General Surgery Huashan HospitalCancer Metastasis InstituteFudan UniversityShanghaiChina Institutes of Biomedical Sciences Fudan UniversityShanghaiChina

Intercellular cross-talk plays important roles in cancer progression and *** how these cancer cells interact with each other is still largely *** released by tumor cells have been proved to be effective cell-to-cell signal *** explored the functional roles of exosomes in metastasis and the potential prognostic values for hepatocellular carcinoma(HCC).Exosomes were extracted from HCC cells of different metastatic *** metastatic effects of exosomes derived from highly metastatic HCC cells(HMH)were evaluated both in vitro and in *** proteins were identified with iTRAQ mass spectrum and verified in cell lines,xenograft tumor samples,and functional *** released by HMH significantly enhanced the in vitro invasion and in vivo metastasis of low metastatic HCC cells(LMH).S100 calcium-binding protein A4(S100A4)was identified as a functional factor in exosomes derived from HMH.S100A4r,ch exosomes significantly promoted tumor metastasis both in vitro and in vivo compared with S100A4^(rich) exosomes or ***,exosomal S100A4 could induce expression of osteopontin(OPN),along with other tumor metastasis/stemness-related *** S100A4 activated OPN transcription via STAT3 *** patients with high exosomal S100A4 in plasma also had a poorer *** conclusion,exosomes from HMH could promote the metastatic potential of LMH,and exosomal S100A4 is a key enhancer for HCC metastasis,activating STAT3 phosphorylation and up-regulating OPN *** suggested exosomal S100A4 to be a novel prognostic marker and therapeutic target for HCC metastasis.

关键词： S100A4 metastasis STAT3

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Insulin-like growth factor 1-induced enolase 2 deacetylation by HDAC3 promotes metastasis of pancreatic cancer

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1857-1870页

作者： Yan Zheng Chao Wu Jimeng Yang Yue Zhao Huliang Jia Min Xue Da Xu Feng Yang Deliang Fu Chaoqun Wang Beiyuan Hu Ze Zhang Tianen Li Shican Yan Xuan Wang Peter J.Nelson Christiane Bruns Lunxiu Qin qiongzhu dong Department of General Surgery Huashan Hospital&Cancer Metastasis Institute&Institutes of Biomedical SciencesFudan UniversityShanghai 200040China General Visceral and Cancer SurgeryUniversity Hospital of CologneCologne 50937Germany Department of Pancreatic Surgery Pancreatic Disease InstituteHuashan HospitalShanghai Medical CollegeFudan UniversityShanghaiChina Medical Clinic and Policlinic IV Ludwig-Maximilian-University(LMU)MunichGermany

Enolase 2(ENO2)is a key glycolytic enzyme in the metabolic process of glycolysis,but its potential function in pancreatic ductal adenocarcinoma(PDAC)is *** this study,we observed a significant overexpression of ENO2 in PDAC tissues,and its expression was correlated with metastasis and poor prognosis in PDAC patients.K394 was identified as a major acetylation site in ENO2 that regulates its enzymatic activity,cell metabolism and PDAC *** of ENO2 suppressed tumor growth and liver metastasis in ***-expression of wild-type(WT)ENO2,but not the K394 acetylation mimetic mutant,could reverse the decreased tumor *** further characterized histone deacetylase 3(HDAC3)and P300/CBP-associated factor(PCAF)as the potential deacetylase and acetyltransferase for ENO2,***3-mediated deacetylation was shown to lead to ENO2 activation and enhancement of ***,insulin-like growth factor-1(IGF-1)was found to decrease K394 acetylation and stimulate ENO2 activity in a dose-and time-dependent *** PI3K/AKT/mTOR pathway facilitated the phosphorylation of HDAC3 on S424,which promoted K394 deacetylation and activation of ***,an oral small-molecule inhibitor of IGF-1R,could inhibit IGF-1-induced ENO2 deacetylation by HDAC3 and the PI3K/AKT/mTOR ***,linsitinib showed a different effect on the growth and metastasis of PDAC depending on the overexpression of WT versus K394-mutant *** results reveal a novel mechanism by which acetylation negatively regulates ENO2 activity in the metastasis of PDAC by modulating *** of IGF-1-induced ENO2 deacetylation represents a promising strategy to prevent the development of PDAC.

关键词： HDAC3 metastasis metabolism

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肝细胞性肝癌组织浸润淋巴细胞表型与分布研究

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中国肿瘤临床 2015年第11期42卷 559-563页

作者：史炯董琼珠钦伦秀孙海晶贾户亮南京大学附属鼓楼医院病理科南京市210008 复旦大学生物医学研究院复旦大学附属中山医院肝外科

目的:肝细胞性肝癌组织浸润淋巴细胞与外周血T细胞表型可能与肿瘤进展及预后相关,本研究检测肝癌患者组织及外周血T细胞表型与分布,分析淋巴细胞表型变化与预后的关系。方法:分析2007年10月至12月中山医院147例肝癌及癌旁组织浸润淋巴... 详细信息

目的:肝细胞性肝癌组织浸润淋巴细胞与外周血T细胞表型可能与肿瘤进展及预后相关,本研究检测肝癌患者组织及外周血T细胞表型与分布,分析淋巴细胞表型变化与预后的关系。方法:分析2007年10月至12月中山医院147例肝癌及癌旁组织浸润淋巴细胞表型(T细胞或B细胞表面标志物:CD3、CD8、CD4、CD20、CD19、Foxp3),表型与临床病理特征及预后的关系;检测26例肝癌外周血CD3、CD8、CD4+T细胞数量并其比例变化。结果:癌巢内肿瘤浸润细胞明显少于癌周组织(P<0.01),癌周淋巴细胞主要分布于癌旁正常肝组织、汇管区,其与患者肝炎病史及肝硬化相关,表型以CD3+T细胞为主,其中又以CD8+细胞毒性T细胞为主;CD4染色在多数病例为阴性,Foxp3仅在个别病例(15/109)呈阳性。肿瘤浸润淋巴细胞B细胞标志CD20、CD19均为阴性。肿瘤组织内CD8+T细胞浸润数量与预后正相关,而癌周浸润淋巴细胞数目与患者转移及复发无显著关系。结论:肝癌肿瘤浸润细胞在癌巢内明显少于癌周组织,肿瘤及癌周浸润细胞以CD8+细胞毒性T细胞为主。肿瘤组织内CD8+T细胞浸润数量与预后相关,而癌周浸润淋巴细胞数量与患者转移及复发无显著关系。

关键词：肿瘤浸润淋巴细胞肝癌表型预后

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肿瘤研究与临床 2017年第8期29卷 505-509页

作者：孙浩然张钰杜鲁巴董琼珠钦伦秀复旦大学附属华山医院普外科上海200040 复旦大学肿瘤转移研究所上海200040 复旦大学生物医学研究院上海200032

目的建立肝癌肿瘤相关成纤维细胞（CAF）分离、培养体系,并予以鉴定,同时进一步探讨CAF对肝癌细胞生物学功能的影响.方法肝细胞癌（HCC）术后患者的肿瘤组织通过胶原酶消化、离心、重悬等技术手段,分离、纯化CAF.分别通过形态学观察... 详细信息

目的建立肝癌肿瘤相关成纤维细胞（CAF）分离、培养体系,并予以鉴定,同时进一步探讨CAF对肝癌细胞生物学功能的影响.方法肝细胞癌（HCC）术后患者的肿瘤组织通过胶原酶消化、离心、重悬等技术手段,分离、纯化CAF.分别通过形态学观察及免疫荧光技术对CAF进行鉴定.在此基础上将分离鉴定的CAF与肝癌细胞株Huh7、HepG2进行共培养,建立CAF与肝癌细胞株体外共培养系统,同时利用CCK-8实验观察CAF对Huh7、HepG2细胞增殖的影响;利用Transwell实验分析CAF对Huh7、HepG2细胞侵袭能力的影响.结果分离、培养成功的CAF形态学表现为长梭状或纺锤状,细胞体积与细胞核较其他细胞明显偏大.免疫荧光结果显示CAF特殊标志物α平滑肌肌动蛋白（α-SMA）和纤维连接蛋白均呈强阳性,并主要表现为胞膜染色.而肝癌细胞表面的特殊标志物甲胎蛋白（AFP）及血管内皮细胞表面特殊标志物CD31均阴性.Huh7、HepG2的增殖和侵袭能力明显增强.其中CAF与Huh7和HepG2细胞共培养24 h后,空白组与实验组中的细胞增殖率分别为（63±4）%、（78±5）%和（69±5）%、（81±3）%,差异均有统计学意义（均P〈0.05）.CAF增强Huh7和HepG2穿膜能力,空白组与实验组中的穿膜细胞数目分别为（59.4±3.1）、（162.9±3.9）个和（104.8±2.6）、（166.4±4.2）个,差异均有统计学意义（均P〈0.05）.结论 HCC患者肿瘤组织中分离、培养的细胞为***形态结构及蛋白表达等具有特异性,并促进肝癌细胞的增殖和侵袭.

关键词：成纤维细胞肝肿瘤平滑肌肌球蛋白细胞增殖肿瘤侵润

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