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Targeting cancer cell plasticity by HDAC inhibition to reverse EBV-induced dedifferentiation in nasopharyngeal carcinoma

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Signal Transduction and Targeted Therapy 2021年第10期6卷 3045-3061页

作者： Jiajun Xie Zifeng Wang Wenjun Fan Youping liu Fang liu Xiangbo Wan Meiling liu Xuan Wang Deshun Zeng Van Wang Bin He Min Yan Zijian Zhang Mengjuan Zhang Zhijie Hou Chunli Wang Zhijie Kang Wenfeng Fang Li Zhang Eric W-F Lam Xiang Guo Jinsong Yan Yixin Zeng Mingyuan Chen quentin liu Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and TherapyGuangzhouChina Institute of Cancer Stem Cell Cancer CenterDalian Medical UniversityDalianChina Department of Hematology Liaoning Key Laboratory of Hematopoietic Stem Cell Transplantation and Translational MedicineLiaoning Medical Center for Hematopoietic Stem Cell TransplantationDalian Key Laboratory of HematologyDiamond Bay Institute of HematologyThe Affiliated Second Hospital of Dalian Medical UniversityDalianChina Department of Radiation Oncology The Sixth Affiliated Hospital of Sun Yat-sen UniversityGuangzhouChina Sun Yat-sen Institute of Hematology The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouChina

Application of differentiation therapy targeting cellular plasticity for the treatment of solid malignancies has been *** carci noma(NPC)is a distinctive cancer with poor differe ntiatio n and high prevalenee of Epstein-Barr virus(EBV)***,we show that the expressi on of EBV latent protein LMP1 in duces dediffere ntiated and stem-like status with high plasticity through the transcriptional inhibition of ***,LMP1 upregulates STAT5A and recruits HDAC 1/2 to the CEBPA locus to reduce its histone *** inhibition restored CEBPA expression,reversing cellular dedifferentiation and stem-like status in mouse xeno graft *** fin dings provide a novel mecha nistic epigenetic-based in sight into virus-induced cellular plasticity and propose a promising concept of differentiation therapy in solid tumor by using HDAC inhibitors to target cellular plasticity.

关键词： LMP1 cancer plasticity

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Cancer cell employs a microenvironmental neural signal transactivating nucleus-mitochondria coordination to acquire stemness

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Signal Transduction and Targeted Therapy 2023年第8期8卷 3818-3836页

作者： Bin He Rui Gao Shasha Lv Ailin Chen Junxiu Huang Luoxuan Wang Yunxiu Feng Jiesi Feng Bing liu Jie Lei Bing Deng Bin He Bai Cui Fei Peng Min Yan Zifeng Wang Eric W-F Lam Bilian Jin Zhiming Shao Yulong Li Jianwei Jiao Xi Wang quentin liu State Key Laboratory of Oncology in South China Sun Yat-sen University Cancer CenterGuangzhou 510060PR China Department of Medical Oncology The Seventh Affiliated HospitalSun Yat-sen UniversityShenzhen 510275PR China Institute of Cancer Stem Cell Cancer CenterDalian Medical UniversityDalian 116023PR China Zhongshan School of Medicine Sun Yat-sen UniversityGuangzhou 510080PR China State Key Laboratory of Membrane Biology Peking University School of Life SciencesBeijing 100871PR China Department of Surgery and Cancer Imperial College LondonLondon W120NNUK Department of Breast Surgery Precision Cancer Medicine CenterFudan University Shanghai Cancer CenterShanghai 200032PR China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101PR China

Cancer cell receives extracellular signal inputs to obtain a stem-like status,yet how tumor microenvironmental(TME)neural signals steer cancer stemness to establish the hierarchical tumor architectures remains ***,a pan-cancer transcriptomic screening for 10852 samples of 33 TCGA cancer types reveals that cAMP-responsive element(CRE)transcription factors are convergent activators for cancer *** of transcriptomic profiles,specification of neural markers and illustration of norepinephrine dynamics uncover a bond between TME neural signals and cancer-cell CRE ***,neural signal norepinephrine potentiates the stemness of proximal cancer cells by activating cAMP-CRE axis,where ATF1 serves as a conserved *** activation by norepinephrine,ATF1 potentiates cancer stemness by coordinated trans-activation of both nuclear pluripotency factors MYC/NANOG and mitochondrial biogenesis regulators NRF1/TFAM,thereby orchestrating nuclear reprograming and mitochondrial ***,single-cell transcriptomes confirm the coordinated activation of nuclear pluripotency with mitochondrial biogenesis in cancer stem-like *** findings elucidate that cancer cell acquires stemness via a norepinephrine-ATF1 driven nucleus-mitochondria collaborated program,suggesting a spatialized stemness acquisition by hijacking microenvironmental neural signals.

关键词： Cancer neural architectures

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Microbiota enterotoxigenic Bacteroides fragilis-secreted BFT-1 promotes breast cancer cell stemness and chemoresistance through its functional receptor NOD1

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Protein & Cell 2024年第6期15卷 419-440页

作者： Wei Ma Lu Zhang Weilong Chen Zhaoxia Chang Juchuanli Tu Yuanyuan Qin Yuwen Yao Mengxue Dong Jiajun Ding Siqin Li Fengkai Li Qiaodan Deng Yifei Yang Tingting Feng Fanrong Zhang Xiying Shao Xueyan He Lixing Zhang Guohong Hu quentin liu Yi-Zhou Jiang Shu Zhu Zhi Xiao Dan Su Tong liu Suling liu Fudan University Shanghai Cancer Center & Institutes of Biomedical Sciences State Key Laboratory of Genetic EngineeringCancer InstitutesDepartment of OncologyKey Laboratory of Breast Cancer in ShanghaiThe Shanghai Key Laboratory of Medical EpigeneticsShanghai Key Laboratory of Radiation OncologyThe International Co-laboratory of Medical Epigenetics and MetabolismMinistry of Science and TechnologyShanghai Medical CollegeFudan UniversityShanghai 200032China Intelligent Pathology Institute and Department of Pathology The First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230071China Department of Thyroid Breast and Vascular SurgeryXijing HospitalFourth Military Medical UniversityXi’an 710032China Institute of Immunology CAS Key Laboratory of Innate Immunity and Chronic DiseaseSchool of Basic Medical SciencesDivision of Life Science and MedicineUniversity of Science and Technology of ChinaHefei 230027China Department of Pathology The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital)Institute of Basic Medicine and Cancer (IBMC)Chinese Academy of SciencesHangzhou 310022China Department of Breast Surgery The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital)Institute of Basic Medicine and Cancer (IBMC)Chinese Academy of SciencesHangzhou 310022China Department of Breast Medical Oncology The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital)Institute of Basic Medicine and Cancer (IBMC)Chinese Academy of SciencesHangzhou 310022China Shanghai Institute of Nutrition and Health University of Chinese Academy of SciencesChinese Academy of SciencesShanghai 200031China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China Department of Breast Surgery Xiangya HospitalChangsha 410008China Department of Breast Surgery Tumor Hospital of Harbin Medic

Tumor-resident microbiota in breast cancer promotes cancer initiation and malignant ***,targeting microbiota to improve the effects of breast cancer therapy has not been investigated in ***,we evaluated the microbiota composition of breast tumors and found that enterotoxigenic Bacteroides fragilis(ETBF)was highly enriched in the tumors of patients who did not respond to taxane-based neoadjuvant ***,albeit at low biomass,secreted the toxic protein BFT-1 to promote breast cancer cell stemness and *** studies showed that BFT-1 directly bound to NOD1 and stabilized NOD1 ***1 was highly expressed on ALDH+breast cancer stem cells(BCSCs)and cooperated with GAK to phosphorylate NUMB and promote its lysosomal degradation,thereby activating the NOTCH1-HEY1 signaling pathway to increase ***1 inhibition and ETBF clearance increase the chemosensitivity of breast cancer by impairing BCSCs.

关键词： NOD1 breast chemotherapy

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超级增强子的转录相分离模型与肿瘤研究进展

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中国细胞生物学学报 2022年第4期44卷 604-614页

作者：雷鑫星刘强中山大学肿瘤防治中心华南肿瘤学国家重点实验室

超级增强子(super-enhancers,SEs)是驱动高转录水平的增强子簇。SEs驱动的基因网络在决定细胞身份方面发挥着重要作用。最近,在SEs驱动的关键癌基因转录模型中引入了相分离(phase separation,PS)的概念。该文系统地讨论了转录PS模型里... 详细信息

超级增强子(super-enhancers,SEs)是驱动高转录水平的增强子簇。SEs驱动的基因网络在决定细胞身份方面发挥着重要作用。最近,在SEs驱动的关键癌基因转录模型中引入了相分离(phase separation,PS)的概念。该文系统地讨论了转录PS模型里的主要元素,通过分子间的作用力总结归纳了元素之间的关系,并讲述了从SEs形成到转录激活延伸的事件。在表观遗传/基因改变下,SEs驱动的癌基因促进肿瘤的发生、进展、转移和耐药。生物物理学学科重新激发了科学家对肿瘤转录调控的思考。

关键词：超级增强子相分离转录癌症(肿瘤)

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Aurora Kinase Small Molecule Inhibitor Destructs Mitotic Spindle,Suppresses Cell Growth,and Induces Apoptosis in Oral Squamous Cancer Cells

Aurora Kinase Small Molecule Inhibitor Destructs Mitotic Spi...

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第八次全国口腔颌面—头颈肿瘤会议

作者： Caobing Pan~1,Hongzhang Huang~1,Min Yan~2,Jine Yao~2,Jie Xu~2,Zijie Long2,quentin liu~2, (1.Department of Maxillofacial Surgery,Second Affiliated Hospital,Sun Yat-sen University,Guangzhou 510120,China 2.State Key Laboratory of Oncology in South China,Cancer Center,Sun Yat-sen University,Guangzhou 510060,China)

Mitotic Aurora kinases are required for accurate chromosome segregation during cell *** expression of Aurora-A (Aur-A) kinase results in centrosome amplification,aberrant spindles,and consequent *** the present study,we showed that Aurora kinase inhibitory small molecule VX-680 inhibited histone H3 phosphorylation at Ser10,a known in vivo substrate residue of Aurora kinase,in oral squamous cell carcinoma(OSCC) KB *** addition,monopolar spindle structures,typical abnormalities induced by inhibition of Aur-A,were generated in VX-680-treated *** of Aurora kinase led to reduced KB cell growth,as assessed by MTT *** blot analysis revealed that VX-680 caused cleavage of two critical apoptotic associated proteins, PARP and *** contrast,expression of cell survival factor Bcl-2 was reduced by VX-680 treatment in a dose-dependent ***,nuclear characteristic of DNA fragmentation,indicative of apoptotic cell death,was clearly observed in these OSCC cells with Aurora kinase inhibitory *** together,we showed that Aurora kinase inhibitory VX-680 led to apoptotic cell death in OSCC cells,suggesting a novel therapeutic target in oral cancer.

关键词： Aur-A,biomarker,molecular target,apoptosis The abbreviations used are:Aur-A,Aurora-A OSCC,Oral squamous cell carcinoma EGFR,Epidermal growth factor receptor BRCA1,Breast Cancer 1 TPX2,Target protein for xklp2 TACC,Transforming acidic coiled-coil Flt3,Fms-like tyrosine kinase 3 Abl Abelson tyrosine kinase

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Extended wet sieving method for determination of complete particle size distribution of general soils

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Journal of Rock Mechanics and Geotechnical Engineering 2024年第1期16卷 242-257页

作者： Shengnan Ma Yi Song Jiawei liu Xingyu Kang Zhongqi quentin Yue Department of Civil Engineering The University of Hong KongHong KongChina

The traditional standard wet sieving method uses steel sieves with aperture?0.063 mm and can only determine the particle size distribution(PSD)of gravel and sand in general *** paper extends the traditional method and presents an extended wet sieving *** extended method uses both the steel sieves and the nylon filter cloth *** apertures of the cloth sieves are smaller than 0.063 mm and equal 0.048 mm,0.038 mm,0.014 mm,0.012 mm,0.0063 mm,0.004 mm,0.003 mm,0.002 mm,and 0.001 mm,*** extended method uses five steps to separate the general soil into many material sub-groups of gravel,sand,silt and clay with known particle size *** complete PSD of the general soil is then calculated from the dry masses of the individual material *** extended method is demonstrated with a general soil of completely decomposed granite(CDG)in Hong Kong,*** silt and clay materials with different particle size ranges are further examined,checked and verified using stereomicroscopic observation,physical and chemical property *** results further confirm the correctness of the extended wet sieving method.

关键词： Particle size distribution(PSD) General soil Silt Clay Wet sieving Physical and chemical properties

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Characterization of glutamatergic VTA neural population responses to aversive and rewarding conditioning in freely-moving mice

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Science Bulletin 2019年第16期64卷 1167-1178页

作者： quentin Montardy Zheng Zhou Zhuogui Lei Xuemei liu Pengyu Zeng Chen Chen Yuanming liu Paula Sanz-Leon Kang Huang Liping Wang Shenzhen Key Lab of Neuropsychiatric Modulation and Collaborative Innovation Center for Brain Science Guangdong Provincial Key Laboratory of Brain Connectome and BehaviorCAS Center for Excellence in Brain Science and Intelligence TechnologyThe Brain Cognition and Brain Disease Institute(BCBDI)Shenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research InstitutionsShenzhen 518055China University of Chinese Academy of Sciences Beijing 100049China School of Physics the University of SydneySydney 2006Australia Centre for Integrative Brain Function the University of SydneySydney 2006Australia Department of Biomedical Sciences City University of Hong KongTat Chee AvenueKowloonHong KongSAR 999077China

The Ventral Tegmental Area(VTA) is a midbrain structure known to integrate aversive and rewarding stimuli, but little is known about the role of VTA glutamatergic(VGluT2) neurons in these *** activation of VGluT2 soma evokes rewarding behaviors, while activation of their downstream projections evokes aversive behaviors. To facilitate our understanding of these conflicting properties, we recorded calcium signals from VTAVGluT2+ neurons using fiber photometry in VGluT2-cre mice to investigate how this population was recruited by aversive and rewarding stimulation, both during unconditioned and conditioned protocols. Our results revealed that, as a population, VTAVGluT2+neurons responded similarly to unconditioned-aversive and unconditioned-rewarding stimulation. During aversive and rewarding conditioning, the CS-evoked responses gradually increased across trials whilst the US-evoked response remained stable. Retrieval 24 h after conditioning, during which mice received only CS presentation, resulted in VTAVGluT2+ neurons strongly responding to CS presentation and to the expected-US but only for aversive conditioning. To help understand these differences based on VTAVGluT2+ neuronal networks, the inputs and outputs of VTAVGluT2+ neurons were investigated using Cholera Toxin B(CTB) and rabies virus. Based on our results, we propose that the divergent VTAVGluT2+ neuronal responses to aversion and reward conditioning may be partly due to the existence of VTAVGluT2+ subpopulations that are characterized by their connectivity.

关键词： Ventral Tegmental Area Aversion Reward Conditioning Behavior

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Activation of parvalbumin interneurons in anterior cingulate cortex impairs observational fear

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Science Bulletin 2018年第12期63卷 771-778页

作者： Chunran Zhou Zheng Zhou Yushui Han Zhuogui Lei Lei Li quentin Montardy Xuemei liu Fuqiang Xu Liping Wang Shenzhen Key Laboratory of Neuropsychiatric Modulation and Collaborative Innovation Center for Brain Science.Guangdong Provincial Key Laboratory of Brain Connectome and Behavior CAS Center for Excellence in Brain Science and Intelligence TechnologyThe Brain Cognition and Brain Disease Institute(BCBDI).Shenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China University of Chinese Academy of Sciences Beijing 100049.China Southern Medical University Guangzhou 510168China Center for Brain Science Key Laboratory of Magnetic Resonance in Biological Systems and State Key Laboratory of Magnetic Resonance and Atomic and Molecular PhysicsWuhan institute of Physics and MathematicsCAS Center for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesWuhan 430071China

The ability to detect conspecific＇s distress is crucial for animal survival. In rodent models, observational fear （OF） occurs when one animal perceives another fear related negative emotions, which may model certain behaviors caused by witnessing traumatic experiences in humans. Anterior cingulate cortex （ACC） has been showed to play a crucial role in OF. However, cellular and neural circuit basis relating to ACC governing OF is poorly understood. Here, we used Designer Receptor Exclusively Activated by a Designer Drug （DREADD） system to investigate the cell type specific circuit mechanism of ACC in OF. Firstly, inhibitory hM4D （Gi） designer receptor together with clozapine N-oxide （CNO） injection was applied to inactivate ACC neurons in the observer mice. We found that, chemogenetic inhibition of ACC resulted in a decreased freezing response in the observer mice. Next, combining PV-ires-Cre mice and Cre-dependent DREADD system, we selectively targeted the ACC parvalbumin （PV） interneurons with the excitatory hM3D （Gq） designer receptor. Activation of ACC PV interneurons following CNO injection reduced freezing response in the observer mice, while had no effect on freezing response in the demon- strator mice. Finally, monosynaptic rabies retrograde tracing revealed that ACC PV interneurons receive inputs from the mediodorsal thalamic nucleus （MD） and the ventromedial thalamic nucleus （VM）, both known for their roles in OF. Taken together, these findings reveal that ACC activation is important for OF, during which PV interneurons in ACC play an important regulatory role. Abnormal function of ACC PV interneurons might contribute to the pathology of empathy- deficits related diseases, such as autism and schizoohrenia.

关键词： Observational fear learning Anterior cingulate cortex PV interneurons Empathy

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Preoperative biliary drainage in patients with hilar cholangiocarcinoma undergoing major hepatectomy

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World Journal of Gastroenterology 2013年第46期19卷 8731-8739页

作者： Jun-Jie Xiong quentin M Nunes Wei Huang Samir Pathak Ai-Lin Wei Chun-Lu Tan Xu-Bao liu Department of Hepato-Biliary-Pancreatic Surgery West China HospitalSichuan University NIHR Liverpool Pancreas Biomedical Research Unit Department of Molecular and Clinical Cancer MedicineRoyal Liverpool University HospitalUniversity of Liverpool Sichuan Provincial Pancreatitis Center Department of Integrated Traditional Chinese and Western MedicineWest China HospitalSichuan University

AIM:To investigate the effect of preoperative biliary drainage(PBD)in jaundiced patients with hilar cholangiocarcinoma(HCCA)undergoing major liver ***:An observational study was carried out by reviewing a prospectively maintained database of HCCA patients who underwent major liver resection for curative therapy from January 2002 to December *** were divided into two groups based on whether PBD was performed:a drained group and an undrained *** baseline characteristics,preoperative factors,perioperative and short-term postoperative outcomes were compared between the two *** factors for postoperative complications were also analyzed by logistic regression test with calculating OR and 95%***:In total,78 jaundiced patients with HCCA underwent major liver resection:32 had PBD prior to operation while 46 did not have *** two groups were comparable with respect to age,sex,body mass index and ***,there was no significant difference in the total bilirubin(TBIL)levels between the drained group and the undrained group at admission(294.2±135.7 vs 254.0±63.5,P=0.126).PBD significantly improved liver function,reducing not only the bilirubin levels but also other liver *** preoperative TBIL level was significantly lower in the drained group as compared to the undrained group(108.1±60.6 vs 265.7±69.1,P=0.000).The rate of overall postoperative complications(53.1%vs 58.7%,P=0.626),reoperation rate(6.3%vs 6.5%,P=1.000),postoperative hospital stay(16.5 vs 15.0,P=0.221)and mortality(9.4%vs 4.3%,P=0.673)were similar between the two *** addition,there was no significant difference in infectious complications(40.6%vs 23.9%,P=0.116)and noninfectious complications(31.3%vs 47.8%,P=0.143)between the two *** and multivariate analyses revealed that preoperative TBIL>170μmol/L(OR=13.690,95%CI:1.275-147.028,P=0.031),Bismuth-Corlette classification(OR=0.013,95%CI:0.001-0.166,P=0.001)and extended

关键词： Obstructive jaundice Hilar cholangiocar-cinoma Preoperative biliary drainage Major hepatec-tomy Surgical outcome

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The root-knot nematode effectorMi2G02 hijacks a host plant trihelix transcription factor to promote nematode parasitism

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Plant Communications 2024年第2期5卷 151-168页

作者： Jianlong Zhao Kaiwei Huang Rui liu Yuqing Lai Pierre Abad Bruno Favery Heng Jian Jian Ling Yan Li Yuhong Yang Bingyan Xie Michael quentin Zhenchuan Mao State Key Laboratory of Vegetable Biobreeding Institute of Vegetables and FlowersChinese Academy of Agricultural SciencesBeijing 100081China INRAE Universite´Cote d’AzurCNRSISA06903 Sophia AntipolisFrance Department of Plant Pathology and Key Laboratory of Pest Monitoring and Green Management of the Ministry of Agriculture China Agricultural UniversityBeijing 100193China

Root-knot nematodes(RKNs)cause huge agricultural losses every *** secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells,which serve as their sole source of ***,the mode of action of these effectors and their targeted host pro-teins remain largely *** this study,we investigated the role of the effector Mi2G02 in Meloidogyne incognita ***-derived Mi2G02 RNA interference in Arabidopsis thaliana affected giant cell development,whereas ectopic expression of Mi2G02 promoted root growth and increased plant sus-ceptibility to *** used various combinations of approaches to study the specific interactions between Mi2G02 and *** GT-3a,a trihelix transcription ***-3a knockout in *** affected feeding-site development,resulting in production of fewer egg masses,whereas GT-3a overex-pression in *** increased susceptibility to *** and also root ***,we demon-strated that Mi2G02 plays a role in maintaining GT-3a protein stabilization by inhibiting the 26S proteasome-dependent pathway,leading to suppression of TOZ and RAD23C expression and thus promoting nematode *** work enhances our understanding of how a pathogen effector manipulates the role and regulation of a transcription factor by interfering with a proteolysis pathway to reprogram gene expression for development of nematode feeding cells.

关键词： Meloidogyne incognita effector giant cell Mi2G02 transcription factor interaction

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