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IL4I1-driven AHR signature: a new avenue for cancer therapy

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Signal Transduction and Targeted therapy 2021年第4期6卷 1086-1087页

作者： Zuli Wang Tiansheng Li Chao Mao Wenliang Liu Yongguang Tao NHC key laboratory of Carcinogenesis and hunan key laboratory of Cancer Metabolism Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of MedicineCentral South UniversityChangshaHunanChina key laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education Cancer Research InstituteCentral South UniversityChangshaHunanChina Department of Thoracic Surgery Hunan Key Laboratory of Early Diagnosis and Precision Therapy in Lung CancerSecond Xiangya HospitalCentral South UniversityChangshaHunanChina

Aryl hydrocarbon receptor(AHR)was considered to be an important pan-tumor therapeutic target,but small molecule inhibitors targeting AHR target gene ID01 have failed in clinical trials.The recent paper published in Ce... 详细信息

关键词： signature explained identif

Immunometabolism:a new dimension in immunotherapy resistance

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Frontiers of Medicine 2023年第4期17卷 585-616页

作者： Chaoyue Xiao Wei Xiong Yiting Xu Ji’an Zou Yue Zeng Junqi Liu Yurong Peng Chunhong Hu Fang Wu Department of Oncology The Second Xiangya HospitalCentral South UniversityChangsha 410011China NHC key laboratory of Carcinogenesis and key laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education Cancer Research InstituteCentral South UniversityChangsha 410078China Xiangya School of Medicine Central South UniversityChangsha 410013China hunan Cancer Mega-Data Intelligent Application and Engineering Research Centre Changsha 410011China Hunan Key Laboratory of Early Diagnosis and Precision Therapy in Lung Cancer The Second Xiangya HospitalCentral South UniversityChangsha 410011China hunan key laboratory of Tumor Models and Individualized Medicine The Second Xiangya HospitalCentral South UniversityChangsha 410011China

Immune checkpoint inhibitors(ICIs)have demonstrated unparalleled clinical responses and revolutionized the paradigm of tumor treatment,while substantial patients remain unresponsive or develop resistance to ICIs as a single agent,which is traceable to cellular metabolic dysfunction.Although dysregulated metabolism has long been adjudged as a hallmark of tumor,it is now increasingly accepted that metabolic reprogramming is not exclusive to tumor cells but is also characteristic of immunocytes.Correspondingly,people used to pay more attention to the effect of tumor cell metabolism on immunocytes,but in practice immunocytes interact intimately with their own metabolic function in a way that has never been realized before during their activation and differentiation,which opens up a whole new frontier called immunometabolism.The metabolic intervention for tumor-infiltrating immunocytes could offer fresh opportunities to break the resistance and ameliorate existing ICI immunotherapy,whose crux might be to ascertain synergistic combinations of metabolic intervention with ICIs to reap synergic benefits and facilitate an adjusted anti-tumor immune response.Herein,we elaborate potential mechanisms underlying immunotherapy resistance from a novel dimension of metabolic reprogramming in diverse tumor-infiltrating immunocytes,and related metabolic intervention in the hope of offering a reference for targeting metabolic vulnerabilities to circumvent immunotherapeutic resistance.

关键词： immune cell immunometabolism metabolic reprogramming immunotherapy resistance tumor microenvironment immune checkpoint inhibitor

Regulating tumor suppressor genes:post-translational modifications

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Signal Transduction and Targeted therapy 2020年第1期5卷 1688-1712页

作者： Ling Chen Shuang Liu Yongguang Tao key laboratory of Carcinogenesis and Cancer Invasion Ministry of EducationDepartment of PathologyXiangya HospitalSchool of Basic MedicineCentral South University410078 ChangshaHunanChina NHC key laboratory of Carcinogenesis(Central South University) Cancer Research InstituteCentral South University410078 ChangshaHunanChina Department of Oncology Institute of Medical SciencesNational Clinical Research Center for Geriatric DisordersXiangya HospitalCentral South University410008 ChangshaHunanChina Hunan Key Laboratory of Early Diagnosis and Precision Therapy Department of Thoracic SurgerySecond Xiangya HospitalCentral South University410011 ChangshaChina

Tumor suppressor genes cooperate with each other in tumors.Three important tumor suppressor proteins,retinoblastoma(Rb),p53,phosphatase,and tensin homolog deleted on chromosome ten(PTEN)are functionally associated and they regulated by posttranslational modification(PTMs)as well.PTMs include phosphorylation,SUMOylation,acetylation,and other novel modifications becoming growing appreciated.Because most of PTMs are reversible,normal cells use them as a switch to control the state of cells being the resting or proliferating,and PTMs also involve in cell survival and cell cycle,which may lead to abnormal proliferation and tumorigenesis.Although a lot of studies focus on the importance of each kind of PTM,further discoveries shows that tumor suppressor genes(TSGs)form a complex“network”by the interaction of modification.Recently,there are several promising strategies for TSGs for they change more frequently than carcinogenic genes in cancers.We here review the necessity,characteristics,and mechanisms of each kind of post-translational modification on Rb,p53,PTEN,and its influence on the precise and selective function.We also discuss the current antitumoral therapies of Rb,p53 and PTEN as predictive,prognostic,and therapeutic target in cancer.

关键词： suppressor translational precise

Rab22a-NeoF1:a promising target for osteosarcoma patients with lung metastasis

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Signal Transduction and Targeted therapy 2020年第1期5卷 1074-1075页

作者： Kai Xie Xinyi Zhang Yongguang Tao key laboratory of Carcinogenesis and Cancer Invasion Ministry of EducationDepartment of PathologyXiangya HospitalCentral South UniversityChangsha410078 HunanChina Hunan Key Laboratory of Early Diagnosis and Precision Therapy Department of Thoracic SurgeryThe Second Xiangya HospitalCentral South UniversityChangsha410011 HunanChina Department of Neurosurgery Xiangya HospitalCentral South UniversityChangsha410008 HunanChina Department of Cardiovascular Medicine Xiangya HospitalCentral South UniversityChangsha410008 HunanChina Department of Cardiovascular Medicine Third Xiangya HospitalCentral South UniversityChangsha410013 HunanChina NHC key laboratory of Carcinogenesis(Central South University) Cancer Research Institute and School of Basic MedicineHunan Key Laboratory of Oncotarget GeneCentral South UniversityChangsha410078 HunanChina

Osteosarcoma is the most common primary malignant bone tumor among adolescents and children,with high level of lung metastasis and poor prognosis.The treatment of metastatic cases remains a challenge in the clinic,leading to the dramatically decreased survival rate.However,the molecular mechanisms are still unclear.A recent article by Kang et al.demonstrated how chromosomal translocations in osteosarcoma facilitated lung metastasis,and shed new light on its therapeutic strategies1(Fig.1).

关键词： metastasis osteosarcoma lung

The cross-talk between methylation and phosphorylation in lymphoid-specific helicase drives cancer stem-like properties

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Signal Transduction and Targeted therapy 2020年第1期5卷 670-683页

作者： Na Liu Rui Yang Ying Shi Ling Chen Yating Liu Zuli Wang Shouping Liu Lianlian Ouyang Haiyan Wang Weiwei Lai Chao Mao Min Wang Yan Cheng Shuang Liu Xiang Wang Hu Zhou Ya Cao Desheng Xiao Yongguang Tao Department of Pathology Key Laboratory of Carcinogenesis and Cancer Invasion(Ministry of Education)Xiangya HospitalCentral South University410078 HunanChina NHC key laboratory of Carcinogenesis(Central South University) Cancer Research Institute and School of Basic MedicineCentral South University410078 ChangshaHunanChina Postdoctoral Research Workstation Department of NeurosurgeryXiangya HospitalCentral South University410078 HunanChina Department of Oncology Institute of Medical SciencesNational Clinical Research Center for Geriatric DisordersXiangya HospitalCentral South University410008 ChangshaHunanChina Xiangya School of Pharmaceutical Sciences Central South University410078 ChangshaChina hunan key laboratory of Tumor Models and Individualized Medicine Hunan Key Laboratory of Early Diagnosis and Precision Therapy in Lung CancerDepartment of Thoracic SurgerySecond Xiangya HospitalCentral South University410011 ChangshaChina Shanghai Institute of Material Medical Chinese Academy of Sciences(CAS)555 Zuchongzhi RoadZhangjiang Hi-Tech Park201203 ShanghaiChina

Posttranslational modifications(PTMs)of proteins,including chromatin modifiers,play crucial roles in the dynamic alteration of various protein properties and functions including stem-cell properties.However,the roles of Lymphoid-specific helicase(LSH),a DNA methylation modifier,in modulating stem-like properties in cancer are still not clearly clarified.Therefore,exploring PTMs modulation of LSH activity will be of great significance to further understand the function and activity of LSH.Here,we demonstrate that LSH is capable to undergo PTMs,including methylation and phosphorylation.The arginine methyltransferase PRMT5 can methylate LSH at R309 residue,meanwhile,LSH could as well be phosphorylated by MAPK1 kinase at S503 residue.We further show that the accumulation of phosphorylation of LSH at S503 site exhibits downregulation of LSH methylation at R309 residue,which eventually promoting stem-like properties in lung cancer.Whereas,phosphorylation-deficient LSH S503A mutant promotes the accumulation of LSH methylation at R309 residue and attenuates stem-like properties,indicating the critical roles of LSH PTMs in modulating stem-like properties.Thus,our study highlights the importance of the crosstalk between LSH PTMs in determining its activity and function in lung cancer stem-cell maintenance.

关键词： cancer residue phosphorylation

CDK11 negatively regulates Wnt/β-catenin signaling in the endosomal compartment by affecting microtubule stability

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Cancer Biology & Medicine 2020年第2期17卷 328-342页

作者： Danmin Ou Lin Chen Jiang He Zhuoxian Rong Jie Gao Liyu Liu Feiyu Tang Jiang Li Yuezhen Deng Lunquan Sun Department of Oncology Center for Molecular MedicineXiangya HospitalCentral South UniversityChangsha 410008China international Cooperation Base of Cancer precision therapy Department of Science and Technology of Hunan ProvinceChangsha 410008China key laboratory of Molecular Radiation Oncology of hunan Province Changsha 410008China National Clinical Research Center for Geriatric Disorders Changsha 410008China

Objectives:Improper activation of Wnt/β-catenin signaling has been implicated in human diseases.Beyond the well-studied glycogen synthase kinase 3p(GSK3p)and casein kinase 1(CK1),other kinases affecting Wnt/β-catenin signaling remain to be defined.Methods:To identify the kinases that modulate Wnt/β-catenin signaling,we applied a kinase small interfering RNA(siRNA)library screen approach.Luciferase assays,immunoblotting,and real-time polymerase chain reaction(PCR)were performed to confirm the regulation o f the Wnt/β-catenin signaling pathway by cyclin-dependent kinase 11(CDK11)and to investigate the underlying mechanism.Confocal immunofluorescence,coimmunoprecipitation(co-IP),and scratch wound assays were used to demonstrate colocalization,detect protein interactions,and explore the function of CDK11.Results:CDK11 was found to be a significant candidate kinase participating in the negative control of Wnt/P-catenin signaling.Down-regulation of CDK11 led to the accumulation of Wnt/β-catenin signaling receptor complexes,in a manner dependent on intact adenomatosis polyposis coli(APC)protein.Further analysis showed that CDK11 modulation of Wnt/P-catenin signaling engaged the endolysosomal machinery,and CDK11 knockdown enhanced the colocalization of Wnt/β-catenin signaling receptor complexes with early endosomes and decreased colocalization with lysosomes.Mechanistically,CDK11 was found to function in Wnt/β-catenin signaling by regulating microtubule stability.Depletion of CDK11 down-regulated acetyl-a-tubulin.Moreover,co-IP assays demonstrated that CDK11 interacts with the a-tubulin deacetylase SIRT2,whereas SIRT2 down-regulation in CDK11-depleted cells reversed the accumulation of Wnt/(3-catenin signaling receptor complexes.CDK11 was found to suppress cell migration through altered W nt/β-catenin signaling.Conclusions:CDK11 is a negative modulator of Wnt/β-catenin signaling that stabilizes microtubules,thus resulting in the dysregulation of receptor complex trafficking from early endosomes to lysosomes.

关键词： Wnt/β-catenin signaling CDK11 endosome microtubule SIRT2

Neoadjuvant therapy for resectable pancreatic cancer:a narrative review

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Journal of Pancreatology 2022年第2期5卷 69-77页

作者： Chengfang Wang Yingsheng Wu Weilin Wang Department of Hepatobiliary and Pancreatic Surgery The Second Affiliated HospitalZhejiang University School of MedicineHangzhouChina key laboratory of precision diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province HangzhouChina Research Center of diagnosis and Treatment Technology for Hepatocellular Carcinoma of Zhejiang Province HangzhouChina Clinical Medicine Innovation Center of precision diagnosis and Treatment for Hepatobiliary and Pancreatic Disease of Zhejiang University HangzhouChina Clinical Research Center of Hepatobiliary and Pancreatic Diseases of Zhejiang Province HangzhouChina Cancer Center Zhejiang UniversityHangzhouChina

The use of neoadjuvant therapy(NAT)for pancreatic ductal adenocarcinoma remains controversial and limited.Therefore,this literature review aimed to assess the feasibility,safety,and efficacy of this treatment.A database search of peer-reviewed articles published in English between January 1990 and June 2021 in PubMed,MEDLINE,and the Web of Science was performed.Original articles,review articles,and meta-analyses relevant to the topic were selected.We found 2 to 4 cycles with FOLFIRINOX,gemcitabine plus nab-paclitaxel,gemcitabine plus S-1,or gemcitabine alone were the most acceptable treatments.Considering the risk of adverse events and cancer progression,NAT is considered safe and tolerable,with a comparable resection rate.Although NAT can result in moderate tumor responses and some extent of local control(improvement of complete resection rate and negative lymph node metastases),no obvious survival benefit is observed.To date,the survival benefits of NAT for resectable pancreatic ductal adenocarcinoma have been very limited.It is too early to say that NAT is the best treatment option for resectable pancreatic cancer.

关键词： Chemotherapy Neoadjuvant therapy Pancreatic cancer Pancreatic ductal adenocarcinoma Preoperative therapy Resectable pancreatic cancer

Hereditary severe insulin resistance syndrome:Pathogenesis,pathophysiology,and clinical management

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Genes & Diseases 2023年第5期10卷 1846-1856页

作者： Junaid Iqbal Hong-Li Jiang Hui-Xuan Wu Long Li Ying-Hui Zhou Nan Hu Fen Xiao Ting Wang Shi-Na Xu Hou-De Zhou National Clinical Research Center for Metabolic Diseases Hunan Provincial Key Laboratory for Metabolic Bone Diseasesand Department of Endocrinology and MetabolismThe Second XiangYa Hospital of Central South UniversityChangshaHunan 410011China

Severe insulin resistance has been linked to some of the most globally prevalent disorders,such as diabetes mellitus,nonalcoholic fatty liver disease,polycystic ovarian syndrome,and hypertension.Hereditary severe insulin resistance syndrome(H-SIRS)is a rare disorder classified into four principal categories:primary insulin receptor defects,lipodystrophies,complex syndromes,and obesity-related H-SIRS.Genes such as INSR,AKT2,TBC1D4,AGPAT2,BSCL2,CAV1,PTRF,LMNA,PPARG,PLIN1,CIDEC,LIPE,PCYT1A,MC4R,LEP,POMC,SH2B1,RECQL2,RECQL3,ALMS1,PCNT,ZMPSTE24,PIK3R1,and POLD1 have been linked to H-SIRS.Its clinical features include insulin resistance,hyperglycemia,hyperandrogenism,severe dyslipidemia,fatty liver,abnormal topography of adipose tissue,and low serum leptin and adiponectin levels.diagnosis of H-SIRS is based on the presence of typical clinical features associated with the various H-SIRS forms and the identification of mutations in H-SIRS-linked genes by genetic testing.Diet therapy,insulin sensitization,exogenous insulin therapy,and leptin replacement therapy have widely been adopted to manage H-SIRS.The rarity of H-SIRS,its highly variable clinical presentation,refusal to be tested for genetic mutations by patients’family members who are not severely sick,unavailability of genetic testing,and testing expenses contribute to the delayed or underdiagnoses of H-SIRS.early diagnosis facilitates early management of the condition,which results in improved glycemic control and delayed onset of diabetes and other complications related to severe insulin resistance.The use of updated genetic sequencing technologies is recommended,and long-term studies are required for genotype–phenotype differentiation and formulation of diagnostic and treatment protocols.

关键词： Diabetes Genetics Insulin resistance Lipodystrophy Pathophysiology therapy

Artificial intelligence for assisting cancer diagnosis and treatment in the era of precision medicine

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Cancer Communications 2021年第11期41卷 1100-1115页

作者： Zi-Hang Chen Li Lin Chen-Fei Wu Chao-Feng Li Rui-Hua Xu Ying Sun Department of Radiation Oncology State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and TherapySun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China Zhongshan School of Medicine Sun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Artificial Intelligence laboratory State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and TherapySun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China Department of Medical Oncology State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and TherapySun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China

Over the past decade,artificial intelligence(AI)has contributed substantially to the resolution of various medical problems,including cancer.Deep learning(DL),a subfield of AI,is characterized by its ability to perform automated feature extraction and has great power in the assimilation and evaluation of large amounts of complicated data.On the basis of a large quantity of medical data and novel computational technologies,AI,especially DL,has been applied in various aspects of oncology research and has the potential to enhance cancer diagnosis and treatment.These applications range from early cancer detection,diagnosis,classification and grading,molecular characterization of tumors,prediction of patient outcomes and treatment responses,personalized treatment,automatic radiotherapy workflows,novel anti-cancer drug discovery,and clinical trials.In this review,we introduced the general principle of AI,summarized major areas of its application for cancer diagnosis and treatment,and discussed its future directions and remaining challenges.As the adoption of AI in clinical use is increasing,we anticipate the arrival of AI-powered cancer care.

关键词： artificial intelligence cancer diagnosis cancer research cancer treatment convolutional neural network deep learning deep neural network oncology