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Aberrant epithelial cell interaction promotes esophageal squamous-cell carcinoma development and progression

Signal Transduction and Targeted Therapy 2024年第1期9卷 279-294页

作者： Liping Chen Shihao Zhu Tianyuan Liu Xuan Zhao Tao Xiang Xiao Hu Chen Wu dongxin lin Department of Etiology and Carcinogenesis National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Key Laboratory of Cancer Genomic Biology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjing 211166China CAMS Oxford Institute Chinese Academy of Medical SciencesBeijing 100006China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China

Epithelial-mesenchymal transition(EMT)and proliferation play important roles in epithelial cancer formation and progression,but what molecules and how they trigger EMT is largely unknown.Here we performed spatial transcriptomic and functional analyses on samples of multistage esophageal squamous-cell carcinoma(ESCC)from mice and humans to decipher these critical issues.By investigating spatiotemporal gene expression patterns and cell–cell interactions,we demonstrated that the aberrant epithelial cell interaction via EFNB1-EPHB4 triggers EMT and cell cycle mediated by downstream SRC/ERK/AKT signaling.The aberrant epithelial cell interaction occurs within the basal layer at early precancerous lesions,which expands to the whole epithelial layer and strengthens along the cancer development and progression.Functional analysis revealed that the aberrant EFNB1-EPHB4 interaction is caused by overexpressedΔNP63 due to TP53 mutation,the culprit in human ESCC tumorigenesis.Our results shed new light on the role of TP53-TP63/ΔNP63-EFNB1-EPHB4 axis in EMT and cell proliferation in epithelial cancer formation.

关键词： esophageal TP53 squamous

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Detection of piRNA-54265 in human serum:evidence and significance

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Cancer Communications 2023年第2期43卷 276-279页

作者： Dongmei Mai Ying Ye Lisha Zhuang Jian Zheng dongxin lin Department of Experimental Research Sun Yat-sen University Cancer CenterState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer MedicineGuangzhouGuangdong 510060P.R.China Department of Etiology and Carcinogenesis National Cancer Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China

Dear Editor,An increasing number of studies have shown that PIWIinteracting RNAs(piRNAs)are aberrantly expressed in many types of human cancer and involved in regulating the malignant progression,piRNAs would be expected to serve as molecular biomarkers for cancer screening and early diagnosis.In a previous study,we have identified the presence of piRNA-54265 in human serum[1].Further research has demonstrated that it is a promising and specific blood molecularmarker for colorectal cancer(CRC)[2].In these studies,we have developed a stem-loop primer reverse transcription-quantitative PCR(RT-qPCR)approach to determine the piRNA-54265 levels,which included the reverse transcription of piRNA-54265 to cDNA using a stem-loop primer and the quantitative detection of cDNA by PCR with the primers and probe specific for piR-54265[2].

关键词： cancer serum colorectal

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Roles and implications of mRNA N^(6)-methyladenosine in cancer

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Cancer Communications 2023年第7期43卷 729-748页

作者： lingxing Zeng Xudong Huang Jialiang Zhang dongxin lin Jian Zheng Department of Experimental Research Sun Yat-sen University Cancer CenterState Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhouGuangdongP.R.China Department of Etiology and Carcinogenesis National Cancer Center/National Clinical Research Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingP.R.China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjingJiangsuP.R.China

RNA N^(6)-methyladenosine modification is the most prevalent internal modification of eukaryotic RNAs and has emerged as a novel field of RNA epigenetics,garnering increased attention.To date,m^(6)A modification has been shown to impact multiple RNA metabolic processes and play a vital role in numerous biological processes.Recent evidence suggests that aberrant m^(6)A modification is a hallmark of cancer,and it plays a critical role in cancer development and progression through multiple mechanisms.Here,we review the biological functions of mRNA m^(6)A modification in various types of cancers,with a particular focus on metabolic reprogramming,programmed cell death and tumor metastasis.Furthermore,we discuss the potential of targetingm^(6)Amodification or its regulatory proteins as a novel approach of cancer therapy and the progress of research on m^(6)A modification in tumor immunity and immunotherapy.Finally,we summarize the development of different m^(6)A detection methods and their advantages and disadvantages.

关键词： cancer therapy immunotherapy m^(6)A methylation N^(6)-methyladenosine

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A cis-eQTL in NSUN2 promotes esophageal squamous-cell carcinoma progression and radiochemotherapy resistance by mRNA-m^(5)C methylation

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Signal Transduction and Targeted Therapy 2022年第9期7卷 3190-3193页

作者： Xiangjie Niu linna Peng Weiling Liu Chuanwang Miao Xinjie Chen Jiahui Chu Xinyu Yang Wen Tan Chen Wu dongxin lin Department of Etiology and Carcinogenesis National Cancer Center/National Clinical Research Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeiingChina CAMS Key Laboratory of Genetics and Genomic Biology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBejingChina Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjingChina

Dear Editor,Esophageal squamous cell carcinoma(ESCC)has poor prognosis because of the difficulty in early detection and low sensitivity of advanced disease to radiochemotherapy.1,2 ESCC presents a high proportion of primary resistance to radiochemotherapy,2which may be due to certain individual genetic variations.Expression quantitative trait loci(eQTLs)as proximal and continuous cellular phenotypes have been shown to be helpful to determine how genetic variants may influence phenotype.

关键词： chemotherapy squamous esophageal

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Multi-omic characterization of genome-wide abnormal DNA methylation reveals diagnostic and prognostic markers for esophageal squamous-cell carcinoma

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Signal Transduction and Targeted Therapy 2022年第3期7卷 896-908页

作者： Yiyi Xi Yuan lin Wenjia Guo Xinyu Wang Hengqiang Zhao Chuanwang Miao Weiling Liu Yachen Liu Tianyuan Liu Yingying Luo Wenyi Fan Ai lin Yamei Chen Yanxia Sun Yulin Ma Xiangjie Niu Ce Zhong Wen Tan Meng Zhou Jianzhong Su Chen Wu dongxin lin Department of Etiology and Carcinogenesis National Cancer Center/National Clinical Research Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Beijing Advanced Innovation Center for Genomics Biomedical Pioneering Innovation CenterPeking UniversityBeijing 100871China Cancer Institute Affiliated Cancer Hospital of Xinjiang Medical UniversityUrumqi 830000China School of Biomedical Engineering School of Ophthalmology and Optometry and Eye HospitalWenzhou Medical UniversityWenzhou 325011China Wenzhou Institute University of Chinese Academy of SciencesWenzhou 325000China Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjing 211166China CAMS Key Laboratory of Genetics and Genomic Biology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China

This study investigates aberrant DNA methylations as potential diagnosis and prognosis markers for esophageal squamous-cell carcinoma(ESCC),which if diagnosed at advanced stages has<30%five-year survival rate.Comparing genome-wide methylation sites of 91 ESCC and matched adjacent normal tissues,we identified 35,577 differentially methylated CpG sites(DMCs)and characterized their distribution patterns.

关键词： esophageal squamous diagnosis

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Genetic polymorphisms in genes regulating cell death and prognosis of patients with rectal cancer receiving postoperative chemoradiotherapy

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Cancer Biology & Medicine 2023年第4期20卷 297-316页

作者： Hongxia Chen Luxi Yin Jie Yang Ningxin Ren Jinna Chen Qixuan Lu Ying Huang Yanru Feng Weihu Wang Shulian Wang Yueping Liu Yongwen Song Yexiong Li Jing Jin Wen Tan dongxin lin State Key Laboratory of Molecular Oncology Department of Etiology and CarcinogenesisBeijing Key Laboratory for Carcinogenesis and Cancer PreventionNational Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of Radiation Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China

Objective:The identification of biomarkers for predicting chemoradiotherapy efficacy is essential to optimize personalized treatment.This study determined the effects of genetic variations in genes involved in apoptosis,pyroptosis,and ferroptosis on the prognosis of patients with locally advanced rectal cancer receiving postoperative chemoradiotherapy(CRT).Methods:The Sequenom MassARRAY was used to detect 217 genetic variations in 40 genes from 300 patients with rectal cancer who received postoperative CRT.The associations between genetic variations and overall survival(OS)were evaluated using hazard ratios(HRs)and 95%confidence intervals(CIs)computed using a Cox proportional regression model.Functional experiments were performed to determine the functions of the arachidonate 5-lipoxygenase(ALOX5)gene and the ALOX5 rs702365 variant.Results:We detected 16 genetic polymorphisms in CASP3,CASP7,TRAILR2,GSDME,CASP4,HO-1,ALOX5,GPX4,and NRF2 that were significantly associated with OS in the additive model(P[C]represses ALOX5 transcription and corollary experiments suggested that ALOX5 may promote colon cancer cell growth by mediating an inflammatory response.Conclusions:Polymorphisms in genes regulating cell death may play essential roles in the prognosis of patients with rectal cancer who are treated with postoperative CRT and may serve as potential genetic biomarkers for individualized treatment.

关键词： Rectal neoplasms genetic variation regulated cell death overall survival ALOX5

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Genomic alterations and precise medicine of esophageal squamous cell carcinoma

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Journal of Bio-X Research 2018年第1期1卷 7-11页

作者： Qionghua Cui Chen Wu dongxin lin National Cancer Center/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjingJiangsu ProvinceChina

Human cancer is a complex disease caused by the interaction of multiple genes and environmental factors.It is known that environmental factors such as smoking,drinking,and food carcinogens are implicated in the development of certain types of cancer including esophageal squamous cell carcinoma(ESCC).However,only a small portion of exposed individuals finally developed cancer,indicating that genetic makeup also plays an important role in the tumorigenesis.Genome-wide association studies(GWAS)have found numerous susceptible genes or loci for cancers,providing new ideas and directions for precision prevention and treatment of cancers.With the advances in the field of next-generation sequencing(NGS),the genomic landscapes of many types of human cancer have comprehensively been characterized.Here,we review the progresses of GWAS and NGS in revealing genomic variations of ESCC,one of the most common cancers in China,and discuss the potential applications of these results in precision medicine of ESCC.

关键词： esophageal cancer genomic alteration precise medicine

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超声检测识别CFRP复合材料PTFE夹杂与富树脂缺陷

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航空制造技术 2024年第3期67卷 83-88页

作者：付冬欣林莉张书宁罗忠兵大连理工大学无损检测研究所大连116024

针对碳纤维增强复合材料(Carbon fiber reinforced polymer,CFRP)缺陷试样制作困难且不同夹杂缺陷难识别的问题,采用仿真与试验相结合的方法,开展聚四氟乙烯(PTFE)夹杂与富树脂缺陷超声检测研究。首先建立考虑CFRP层结构弹性各向异性的... 详细信息

针对碳纤维增强复合材料(Carbon fiber reinforced polymer,CFRP)缺陷试样制作困难且不同夹杂缺陷难识别的问题,采用仿真与试验相结合的方法,开展聚四氟乙烯(PTFE)夹杂与富树脂缺陷超声检测研究。首先建立考虑CFRP层结构弹性各向异性的多向层合板超声反射法有限元模型,对比模拟与试验得到的A扫描时域信号,证明了模型的有效性。在CFRP层合板内部设置宽度6 mm,厚度0.03~0.40 mm的PTFE夹杂和厚度0.03~0.85 mm的富树脂缺陷,模拟得到超声A扫描信号,分析比较两种缺陷厚度变化对超声信号幅值最大值和波形峭度因子的影响。结果显示,随着缺陷厚度增加,PTFE夹杂及富树脂缺陷信号的幅值最大值和峭度因子均呈现先上升后下降最后趋于稳定的趋势,但富树脂缺陷信号幅值最大值低于PTFE夹杂,其峭度因子随厚度变化滞后于PTFE夹杂。

关键词：碳纤维增强复合材料(CFRP) 数值模拟缺陷识别 PTFE夹杂富树脂

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Metformin inhibits pancreatic cancer metastasis caused by SMAD4 deficiency and consequent HNF4G upregulation

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Protein & Cell 2021年第2期12卷 128-144页

作者： Chengcheng Wang Taiping Zhang Quan Liao Menghua Dai Junchao Guo Xinyu Yang Wen Tan dongxin lin Chen Wu Yupei Zhao Department of General Surgery Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Etiology and Carcinogenesis National Cancer Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjing 211166China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China CAMS Oxford Institute(COI) Chinese Academy of Medical SciencesBeijing 100730China

Pancreatic ductal adenocarcinoma(PDAC)has poor prognosis due to limited therapeutic options.This study examines the roles of genome-wide association study identified PDAC-associated genes as therapeutic targets.We have identified HNF4G gene whose silencing most effectively repressed PDAC cell invasiveness.HNF4G overexpression is induced by the deficiency of transcriptional factor and tumor suppressor SMAD4.Increased HNF4G are correlated with SMAD4 deficiency in PDAC tumor samples and associated with metastasis and poor survival time in xenograft animal model and in patients with PDAC(log-rank P=0.036;HR=1.60,95%CI=1.03–2.47).We have found that Metformin suppresses HNF4G activity via AMPK-mediated phosphorylation-coupled ubiquitination degradation and inhibits in vitro invasion and in vivo metastasis of PDAC cells with SMAD4 deficiency.Furthermore,Metformin treatment significantly improve clinical outcomes and survival in patients with SMAD4-deficient PDAC(log-rank P=0.022;HR=0.31,95%CI=0.14–0.68)but not in patients with SMAD4-normal PDAC.Pathway analysis shows that HNF4G may act in PDAC through the cell-cell junction pathway.These results indicate that SMAD4 deficiency-induced overexpression of HNF4G plays a critical oncogenic role in PDAC progression and metastasis but may form a druggable target for Metformin treatment.

关键词： pancreatic cancer HNF4G SMAD4 deficiency SMAD4-deficient PDAC Metformin

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Integrative analysis of gene expression profiles reveals specific signaling pathways associated with pancreatic duct adenocarcinoma

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Cancer Communications 2018年第1期38卷 158-169页

作者： Jun Li Wenle Tan linna Peng Jialiang Zhang Xudong Huang Qionghua Cui Jian Zheng Wen Tan Chen Wu dongxin lin Department of Etiology and Carcinogenesis National Cancer Center/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhouGuangdong 510060P.R.China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjingJiangsu 210009P.R.China

Background:Pancreatic duct adenocarcinoma(PDAC)remains a major health problem because conventional can-cer treatments are relatively ineffective against it.Microarray studies have linked many genes to pancreatic cancer,but the available data have not been extensively mined for potential insights into PDAC.This study attempted to identify PDAC-associated genes and signaling pathways based on six microarray-based profiles of gene expression in pancre-atic cancer deposited in the gene expression omnibus database.Methods:Pathway network methods were used to analyze core pathways in six publicly available pancreatic cancer gene(GSE71989,GSE15471,GSE16515,GSE32676,GSE41368 and GSE28735)expression profiles.Genes potentially linked to PDAC were assessed for potential impact on survival time based on data in The Cancer Genome Atlas and International Cancer Genome Consortium databases,and the expression of one candidate gene(CKS2)and its association with survival was examined in 102 patients with PDAC from our hospital.Effects of CKS2 knockdown were explored in the PDAC cell lines BxPC-3 and CFPAC-1.Results:The KEGG signaling pathway called“pathway in cancer”may play an important role in pancreatic cancer development and progression.Five genes(BIRC5,CKS2,ITGA3,ITGA6 and RALA)in this pathway were significantly associated with survival time in patients with PDAC.CKS2 was overexpressed in PDAC samples from our hospital,and higher CKS2 expression in these patients was associated with shorter survival time.CKS2 knockdown substantially inhibited PDAC cell proliferation in vitro.Conclusions:Analysis integrating existing microarray datasets allowed identification of the“pathway in cancer”as an important signaling pathway in PDAC.This integrative approach may be powerful for identifying genes and pathways involved in cancer.

关键词： Pancreatic cancer GEO Pathway network CKS2

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