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Targeting m6a modification inhibits herpes virus 1 infection

Genes & Diseases 2022年第4期9卷 1114-1128页

作者： Zhuoying Feng Fanghang Zhou miaomiao Tan Tingting Wang Ying Chen Wenwen Xu Bin Li Xin Wang Xin Deng ming-Liang He Department of Biomedical Sciences City University of Hong KongKowloonHong KongPR China mOE Key Laboratory of Tumor molecular Biology and Guangdong Provincial Key Laboratory of Bioengineering medicine National Engineering Research Center of Genetic MedicineInstitute of BiomedicineCollege of Life Science and TechnologyJinan UniversityGuangzhouGuangdong 510632PR China CityU Shenzhen Research Institute ShenzhenGuangdong 518057PR China

The latent infection by herpes virus type 1(HSV-1)may be lifelong in trigeminal ganglia and a suspected cause of Alzheimer's Disease(AD)and Amyotrophic lateral sclerosis(ALS).Whether and how N6-methyladenosine(m6a)modification of viral RNAs affects virus infection are poorly ***,we report that HSV-1 infection enhanced the expression of m6a writers(mETTL3,mETTL14)and readers(YTHDF1/2/3)at the early infection stage and decreased their expression later on,while suppressed the erasers'(FTO,ALBKH5)expression immediately upon infection to facilitate viral *** m6a modification by 3-deazaadenosine(DAA)significantly decreased viral replication and reduced viral reproduction over 1000 *** interestingly,depleting the writers and readers by siRNAs inhibited virus replication and reproduction;whereas depleting the erasers promoted viral replication and *** YTHDF3 strikingly decreased viral replication by up to 90%,leading to reduction of up to 10-fold viral replication and over 100-fold virus reproduction,*** of m6a initiator mETTL3(by 60%–70%)by siRNA correlatedly decreased viral replication 60%–70%,and reduced virus yield over ***,ectopic expression of mETTL3 largely increased virus ***3 knockdown suppressed the HSV-1 intermediate early and early genes(ICP0,ICP8 and UL23)and late genes(VP16,UL44,UL49 and ICP47);while ectopic expression of mETTL3 upregulated these gene *** from our study shed the lights on the importance for m6a modification to initiate HSV-1 early *** components of m6a modification machinery,particularly m6a initiator mETTL3 and reader YTHDF3,would be potential important targets for combating HSV-1 infections.

关键词： Gene silencing HSV-1 infection m6a modification Virus replication Virus reproduction

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Epigenetic modifications and metabolic memory in diabetic retinopathy:beyond the surface

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Neural Regeneration Research 2023年第7期18卷 1441-1449页

作者： Dan-Dan Liu Chao-Yang Zhang Jing-Ting Zhang Li-min Gu Guo-Tong Xu Jing-Fa Zhang Department of Ophthalmology of Tongji Hospital Tongji Eye InstituteDepartment of Regenerative Medicineand Department of PharmacologyTongji University School of MedicineShanghaiChina Department of Ophthalmology Shanghai General Hospital(Shanghai First People’s Hospital)Shanghai Jiao Tong UniversityShanghaiChina National Clinical Research Center for Eye Diseases Shanghai Key Laboratory of Ocular Fundus DiseasesShanghai Engineering Center for Visual Science and PhotomedicineShanghai Engineering Center for Precise Diagnosis and Treatment of Eye DiseasesShanghaiChina Department of Ophthalmology Shanghai Aier Eye HospitalShanghaiChina

Epigenetics focuses on DNA methylation,histone modification,chromatin remodeling,noncoding RNAs,and other gene regulation mechanisms beyond the DNA *** the past decade,epigenetic modifications have drawn more attention as they participate in the development and progression of diabetic retinopathy despite tight control of glucose *** underlying mechanisms of epigenetic modifications in diabetic retinopathy still urgently need to be *** diabetic condition facilitates epigenetic changes and influences target gene *** this review,we summarize the involvement of epigenetic modifications and metabolic memory in the development and progression of diabetic retinopathy and propose novel insights into the treatment of diabetic retinopathy.

关键词： diabetic retinopathy DNA methylation epigenetics histone modification metabolic memory m6a modification non-coding RNAs review

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Optimizing ABA-based chemically induced proximity for enhanced intracellular transcriptional activation and modification response to ABA

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Science China Life Sciences 2024年第12期67卷 2650-2663页

作者： Zeng Zhou Yue-Qi Wang Xu-Nan Zheng Xiao-Hong Zhang Lu-Yao Ji Jun-You Han Ze-Cheng Zuo Wei-Liang mo Li Zhang College of Life Sciences Fujian Agriculture and Forestry University Basic Forestry and Proteomics Research Center Fujian Agriculture and Forestry University Jilin Province Engineering Laboratory of Plant Genetic Improvement College of Plant Science Jilin University

Abscisic acid(ABA)-based chemically induced proximity(CIP) is primarily mediated by the interaction of the ABA receptor pyrabactin resistance 1-like 1(PYL1) and the 2C-type protein phosphatase ABI1, which confers ABA-induced proximity to their fusion proteins, and offers precise temporal control of a wide array of biological processes. However, broad application of ABA-based CIP has been limited by ABA response intensity. In this study, we demonstrated that ABA-induced interaction between another ABA receptor pyrabactin resistance 1(PYR1) and ABI1 exhibited higher ABA response intensity than that between PYL1 and ABI1 in HEK293T cells. We engineered PYR1-ABI1and PYL1-ABI1 into ABA-induced transcriptional activation tools in mammalian cells by integration with CRISPR/d Cas9 and found that the tool based on PYR1-ABI1 demonstrated better ABA response intensity than that based on PYL1-ABI1 for both exogenous and endogenous genes in mammalian cells. We further achieved ABA-induced RNA m6a modification installation and erasure by combining ABA-induced PYR1-ABI1 interaction with CRISPR/d Cas13, successfully inhibiting tumor cell proliferation. We subsequently improved the interaction of PYR1-ABI1 through phage-assisted continuous evolution(PACE), successfully generating a PYR1 mutant(PYR1m) whose interaction with ABI1 exhibited a higher ABA response intensity than that of the wild-type. In addition, we tested the transcriptional activation tool based on PYRm-ABI1 and found that it also showed a higher ABA response intensity than that of the wild type. These results demonstrate that we have developed a novel ABA-based CIP and further improved upon it using PACE, providing a new approach for the modification of other CIP systems.

关键词： ABA chemically induced proximity transcriptional activation m6a modification protein evolution

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The crucial roles of m^(6)A RNA modifications in cutaneous cancers:Implications in pathogenesis,metastasis,drug resistance,and targeted therapies

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Genes & Diseases 2023年第6期10卷 2320-2330页

作者： Cong Huang Kaoyuan Zhang Yang Guo Changbing Shen Xiaoming Liu Haiyan Huang Xia Dou Bo Yu Department of Dermatology Skin Research Institute of Peking University Shenzhen HospitalPeking University Shenzhen HospitalShenzhen Peking University-The Hong Kong University of Science and Technology Medical CenterShenzhenGuangdong 518036China Department of Dermatology Skin Research Institute of Peking University Shenzhen HospitalPeking University Shenzhen HospitalShenzhenGuangdong 518036China

N6-methyladenosine(m^(6)A)is the most abundant internal modification on *** is a dynamical and reversible process,which is regulated by m^(6)A methyltransferase and m^(6)A *** m^(6)A modified RNA can be specifically recognized by the m^(6)A reader,leading to RNA splicing,maturation,degradation or *** abnormality of m^(6)A RNA modification is closely related to a variety of biological processes,especially the occurrence and development of *** studies have shown that m^(6)A RNA modification is involved in the pathogenesis of skin ***,the precise molecular mechanisms of m^(6)A-mediated cutaneous tumorigenesis have not been fully ***,this review will summarize the biological characteristics of m^(6)A modification,its regulatory role and mechanism in skin cancers,and the recent research progress of m^(6)A-related molecular drugs,aiming to provide new ideas for clinical diagnosis and targeted therapy of cutaneous cancers.

关键词： Cutaneous squamous cell carcinoma Cutaneous melanoma m6a modification m^(6)A-related drugs Target Therapy

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Ferroptosis:a critical mechanism of N^(6)-methyladenosine modification involved in carcinogenesis and tumor progression

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Science China(Life Sciences) 2024年第6期67卷 1119-1132页

作者： Qingqing Wei Changning Xue mengna Li Jianxia Wei Lemei Zheng Shipeng Chen Yumei Duan Hongyu Deng Faqing Tang Wei Xiong ming Zhou NHC Key Laboratory of Carcinogenesis Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of MedicineCentral South UniversityChangsha 410013China Cancer Research Institute and School of Basic medical Sciences Central South UniversityChangsha 410078China The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese ministry of Education Central South UniversityChangsha 410078China Hunan Key Laboratory of Oncotarget Gene Hunan Key Laboratory of Cancer MetabolismHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of MedicineCentral South UniversityChangsha 410013China

Ferroptosis is an iron-dependent regulatory cell necrosis induced by iron overload and lipid *** occurs when multiple redoxactive enzymes are ectopically expressed or show abnormal ***,the precise regulation of ferroptosis-related molecules is mediated across multiple levels,including transcriptional,posttranscriptional,translational,and epigenetic levels.N^(6)-methyladenosine(m^(6)A)is a highly evolutionarily conserved epigenetic modification in *** m^(6)A modification is commonly linked to tumor proliferation,progression,and therapy resistance because it is involved in RNA metabolic ***,accumulating evidence suggests that dysregulated ferroptosis caused by the m^(6)A modification drives tumor *** this review,we summarized the roles of m^(6)A regulators in ferroptosis-mediated malignant tumor progression and outlined the m^(6)A regulatory mechanism involved in ferroptosis *** also analyzed the potential value and application strategies of targeting m^(6)A/ferroptosis pathway in the clinical diagnosis and therapy of tumors.

关键词： ferroptosis m6a modification RNA methylation m^(6)A regulator tumor progression

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The FTO/miR-181b-3p/ARL5B signaling pathway regulates cell migration and invasion in breast cancer

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Cancer Communications 2020年第10期40卷 484-500页

作者： Yuanyuan Xu Shuang Ye Nan Zhang Shuhui Zheng Huatao Liu Kewen Zhou Ling Wang Yue Cao Peng Sun Tinghuai Wang Department of Physiology Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Research Center for Translational medicine The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Clinical medicine Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Basic medicine Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Pathology State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China

Background:N6-methyladenosine(m6a)RNA modification has been demonstrated to be a significant regulatory process in the progression of various tumors,including breast *** mass and obesity-associated(FTO)enzyme,initially known as the obesity-related protein,is the first identified m6a ***,the relationship between FTO and breast cancer remains *** this study,we aimed to elucidate the role and clinical significance of FTO in breast cancer and to explore the underlying ***:We first investigated the expression of FTO in breast cancer cell lines and tissues by quantitative reverse transcription-PCR(qRT-PCR),Western blotting,and *** healing assay and Transwell assay were performed to determine the migration and invasion abilities of SKBR3 and mDAmB453 cells with either knockdown or overexpression of *** sequencing(RNA-seq)was conducted to decipher the downstream targets of ***-PCR,luciferase reporter assay,and Western blotting were employed to confirm the existence of the FTO/miR-181b-3p/ARL5B *** biological function of ADP ribosylation factor like GTPase 5B(ARL5B)in breast cancer cells was evaluated by wound healing assay and Transwell invasion ***:High FTO expression was observed in human epidermal growth factor receptor 2(HER2)-positive breast cancer,predicting advanced progression(tumor size[Pmoral lymphovascular invasion[Pmph node metastasis[P=0.002],and TNm stage[P=0.001])and poor ***,FTO promoted cell invasion and migration in ***,RNA-seq and further confirmation studies suggested that FTO up-regulated ARL5B by inhibiting *** further verified that ARL5B also displayed carcinogenic activity in breast cancer ***:Our work demonstrated the carcinogenic activity of FTO in promoting the invasion and migration of breast cancer cells via the FTO/miR-181b-3p/ARL5B signaling pathw

关键词： ARL5B breast cancer disease-free survival Fat mass and obesity-associated(FTO)enzyme human epidermal growth factor receptor 2 m6a modification metastasis miR-181b-3p overall survival

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Effect of demethyltransferase FTO on tumor progression

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BIOCELL 2022年第11期46卷 2387-2397页

作者： LING SHENG YUEHONG SHEN HONGYU YANG School of Stomatology Weifang Medical UniversityWeifang261035China Department of Oral and maxillofacial Surgery Shenzhen HospitalPeking UniversityShenzhen518036China

N6-methyladenosine(m6a)modification is the most widespread and conserved internal mRNA modification in mammalian *** greatly affects genetic regulation by enhancing the involvement of diverse cellular enzymes and thus,plays a significant role in basic life *** studies on m6a modification identified FTO as a crucial demethylase that participates in various biological *** only does FTO play a pivotal role in obesity-related conditions,but it also influences the occurrence,development,and prognosis of several cancers,such as acute myeloid leukemia,breast cancer,liver cancer,and lung ***,FTO also shows a close association with immunity and viral *** article summarized the molecular mechanism of FTO in tumorigenesis and tumor progression.

关键词： m6a modification Fat mass and obesity-associated protein molecular functional mechanism

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Recent progress in N6-methyladenosine modification in ocular surface diseases

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International Journal of Ophthalmology(English edition) 2023年第4期16卷 645-651页

作者： Wei Wang Jun Zou Department of Ophthalmology Shanghai Tenth People’s HospitalSchool of MedicineTongji UniversityShanghai 200072China

N6-methyladenosine(m6a)modification is a reversible process promoted by“writers”,inhibited by“erasers”,and processed by“readers”.During the last decade,increasing emphasis has been placed on the underlying roles of m6a modification owing to their great importance in biological *** abnormal regulation of m6a modification will lead to aberrant cellular behavior and various ***,studies have demonstrated that m6a modification is closely associated with the genesis and progression of ocular surface diseases(OSDs).This review focus on the role of m6a modification and research progress in OSDs including fungal keratitis,herpes simplex keratitis,immunerelated keratoconjunctival diseases,pterygium,ocular chemical burns,and Graves’ophthalmopathy,which may provide new insights into and prospective applications for OSDs.

关键词： N6-methyladenosine m6a modification epigenetics ocular surface diseases

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Dysregulation and implications of N6-methyladenosine modification in renal cell carcinoma

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Current Urology 2023年第1期17卷 45-51页

作者： Yaohai Wu Shiqiang Zhang Chujie Chen Jun Pang Department of Urology Kidney and Urology CenterPelvic Floor Disorders CenterThe Seventh Affiliated HospitalSun Yat-sen UniversityShenzhen518107China

Increasing evidence indicates that N6-methyladenosine(m6a)methylation modification serves important functions in biological *** of m6a regulators is related to the progression of different malignancies,including renal cell carcinoma(RCC).Recent studies have reported preliminary findings on the influence of m6a regulator dysregulation on RCC tumorigenesis and ***,no comprehensive review that integrates and analyzes the roles of m6a modification in RCC has been published to *** this review,we focus on the dysregulation of m6a regulators as it relates to RCC tumorigenesis and development,as well as possible applications of m6a modification in RCC diagnosis and therapeutics.

关键词： Dysregulation m6a modification Renal cell carcinoma

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Transcriptomic N6-methyladenosine methylation loss in genes related to cell differentiation conferred by ALKBH5misregulation is a hallmark of colorectal malignancy

Transcriptomic N6-methyladenosine methylation loss in genes ...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Dingcheng Shen Xiaolin Wang Gaopo Xu Heng Wang Yaoyi Huang jinxin Lin Yumo Xie Ziying Huang Zhuokai Zhuang Puning Wang meijin Huang Yanxin Luo Huichuan Yu The Sixth Affiliated Hospital Sun Yat-sen University 中山大学中山医学院

Background: N6-methyladenosine(m6 A) modification is an emerging epigenetic regulatory mechanism in tumorigenesis. Considering that AlkB homolog 5(ALKBH5) is a well-described m6 A demethylase in previous enzyme assays, we aimed to investigate the role of m6 A methylation alteration conferred by disturbed ALKBH5 in colorectal cancer(CRC) ***: Expression of ALKBH5 and its correlation with clinicopathological characteristics of CRC were evaluated using the prospectively maintained institutional database program of colorectal disease(IDPCD). The biological functions and underlying mechanisms of ALKBH5 were explored using in vitro and in vivo experiments. moreover, methylated RNA immunoprecipitation(meRIP), RNA-seq and m6 A dot blot assay were applied to identify the target genes that were regulated by ALKBH5-induced m6 A methylation ***: ALKBH5 expression was significantly upregulated in CRC tissues compared to their adjacent normal tissues. Highly expressed ALKBH5 was found to be independently associated with worse overall survival(adjusted HR 1.63, 95% CI: 1.09-2.43;P = 0.017) after corrected by multiple clinicopathological risk factors. Next, we verified that ALKBH5 could promote CRC cells proliferation, migration and invasion in in-vitro assays, whereas its knockdown produced the opposite effects. Then, we determined the global m6 A level of RNA in the scramble and ALKBH5-knockdown group through m6 A dot blot assay. As expected, m6 A levels were obviously increased after ALKBH5 was silenced in CRC cells. The integrating analysis of meRIP-seq and RNA-seq for ALKBH5-silenced cells found a group of ALKBH5-target genes that were potentially regulated by RNA m6 A modification. Gene Set Enrichment Analysis(GSEA) and Gene ontology(GO) analysis revealed that ALKBH5-target genes were mostly involved in cell differentiation(including ITGAX, TACSTD2,DPEP1, PTP4 A1 and IFIT2).Conclusions: The m6 A methylation loss in cell differentiation-related gene

关键词： ALKBH5 Colorectal cancer m6a modification Hallmark

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