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sirt6 as a key event linking P53 and NRF2 counteracts APAP-induced hepatotoxicity through inhibiting oxidative stress and promoting hepatocyte proliferation

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Acta Pharmaceutica Sinica B 2021年第1期11卷 89-99页

作者： Yanying Zhou Xiaomei Fan Tingying Jiao Wenzhou Li Panpan Chen Yiming Jiang Jiahong Sun Yixin Chen Pan Chen Lihuan Guan Yajie Wen Min Huang Huichang Bi School of Pharmaceutical Sciences Sun Yat-sen UniversityGuangzhou 510006China Shenzhen Baoan Women’s and Children’s Hospital Jinan UniversityShenzhen 518102China Department of Pharmacy the First Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510080China

Acetaminophen(APAP)overdose is the leading cause of drug-induced liver injury,and its prognosis depends on the balance between hepatocyte death and *** 6(sirt6)has been reported to protect against oxidative stress-associated DNA *** whether sirt6 regulates APAPinduced hepatotoxicity remains *** this study,the protein expression of nuclear and total sirt6 was up-regulated in mice liver at 6 and 48 h following APAP treatment,***6 knockdown in AML12 cells aggravated APAP-induced hepatocyte death and oxidative stress,inhibited cell viability and proliferation,and downregulated CCNA1,CCND1 and CKD4 protein ***6 knockdown signifi-cantly prevented APAP-induced NRF2 activation,reduced the transcriptional activities of GSTm andNQO1 and the m RNA levels of Nrf2,Ho-1,Gsta and ***,sirt6 showed potential protein interaction with NRF2 as evidenced by co-immunoprecipitation(Co-IP)***,the protective effect of P53 against APAP-induced hepatocytes injury was *** sirt6 m RNA was significantly down-regulated in P53à/àmice.P53 activated the transcriptional activity of sirt6 and exerted interaction with *** results demonstrate that sirt6 protects against APAP hepatotoxicity through alleviating oxidative stress and promoting hepatocyte proliferation,and provide new insights in the function of sirt6 as a crucial docking molecule linking P53 and NRF2.

关键词： Acetaminophen Hepatotoxicity sirt6 NRF2 P53

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Ellagic acid ameliorates cisplatin-induced acute kidney injury by regulating inflammation and sirt6/TNF-α signaling

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Food Science and Human Wellness 2023年第6期12卷 2232-2241页

作者： Yuqi Gao Kezheng Peng Yida Wang Yannan Guo Chenye Zeng Rui Hua Qingfei Liu Xue Li Ying Qiu Zhao Wang The Ministry of Education Key Laboratory of Protein Science School of Pharmaceutical SciencesTsinghua UniversityBeijing 100084China School of Medicine Tsinghua UniversityBeijing 100084China

De spite cisplatin has been widely used in the treatment of various cancers,the noteworthy nephrotoxicity greatly constrained its clinical *** this reason,finding novel targeted therapies to attenuate the nephrotoxicity of cisplatin should be pretty *** previous study found that histone deacetylase sirtuin 6(sirt6)could be an ideal target for the treatment of cisplatin-induced acute kidney *** this study,we explored the protective effects of ellagic acid,a natural polyphenol compound that activates sirt6,on cisplatin-induced ***-treatment of ellagic acid attenuated cytotoxicity of cisplatin in primary renal cells and TCMK-1 ***,ellagic acid ameliorated renal dysfunction,apoptosis and fibrosis induced by cisplatin in ***,ellagic acid reduced nephrotoxicity-associated inflammatory factor interleukin(IL)-1βand IL-6 expression both in vitro and in ***,ellagic acid reversed cisplatin-reduced sirt6 expression and diminished cisplatin-induced tumor necrosis factor(TNF)-α*** sirt6 knockdown abrogated the protective effects of ellagic acid on cisplatin-induced cell apoptosis,indicating the renal-protective effects of ellagic acid are mainly dependent on ellagic acid-mediated sirt6 *** results provide preclinical rationale for using ellagic acid as a feasible and promising agent to ameliorate cisplatin-induced acute kidney injury,and support ellagic acid as a potential adjunctive therapy for future cancer treatment.

关键词： Ellagic acid Nephrotoxicity Cisplatin sirt6 TNF-α

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Targeting a cryptic allosteric site of sirt6 with small-molecule inhibitors that inhibit the migration of pancreatic cancer cells

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Acta Pharmaceutica Sinica B 2022年第2期12卷 876-889页

作者： Qiufen Zhang Yingyi Chen Duan Ni Zhimin Huang Jiacheng Wei Li Feng Jun-Cheng Su Yingqing Wei Shaobo Ning Xiuyan Yang Mingzhu Zhao Yuran Qiu Kun Song Zhengtian Yu Jianrong Xu Xinyi Li Houwen Lin Shaoyong Lu Jian Zhang State Key Laboratory of Oncogenes and Related Genes Department of PharmacyRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200127China Medicinal Chemistry and Bioinformatics Center Shanghai Jiao Tong University School of MedicineShanghai 200025China Nutshell Therapeutics Shanghai 201203China Academy of Integrative Medicine Shanghai University of Traditional Chinese MedicineShanghai 201203China School of Pharmaceutical Sciences Zhengzhou UniversityZhengzhou 450001China

sirt6 belongs to the conserved NAD^(+)-dependent deacetylase superfamily and mediates multiple biological and pathological *** sirt6 by allosteric modulators represents a novel direction for therapeutics,which can overcome the selectivity problem caused by the structural similarity of orthosteric sites among ***,developing a reversed allosteric strategy Allo Reverse,we identified a cryptic allosteric site,Pocket Z,which was only induced by the bi-directional allosteric signal triggered upon orthosteric binding of NAD^(+).Based on Pocket Z,we discovered an sirt6 allosteric inhibitor named ***-42 selectively targets sirt6 among other histone deacetylases and effectively inhibits sirt6 deacetylation,with an IC50 of 2.33μmol/***-42 significantly suppresses sirt6-mediated cancer cell migration and pro-inflammatory cytokine ***-42,to our knowledge,is the most potent and selective allosteric sirt6 *** study provides a novel strategy for allosteric drug design and will help in the challenging development of therapeutic agents that can selectively bind sirt6.

关键词： sirt6 Molecular dynamics simulations Reversed allostery Allosteric inhibitor Pancreatic cancer Cell migration Cytokine production

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Discovery of a potent and highly selective inhibitor of sirt6 against pancreatic cancer metastasis in vivo

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Acta Pharmaceutica Sinica B 2024年第3期14卷 1302-1316页

作者： Xinyuan Xu Qian Zhang Xufeng Wang Jing Jin Chengwei Wu Li Feng Xiuyan Yang Mingzhu Zhao Yingyi Chen Shaoyong Lu Zhen Zheng Xiaobing Lan Yi Wang Yan Zheng Xuefeng Lu Qiufen Zhang Jian Zhang State Key Laboratory of Medical Genomics National Research Center for Translational Medicine at ShanghaiRuijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China Medicinal Chemistry and BioinformaticsCenter Shanghai Jiao Tong University School of MedicineShanghai 200025China Department of General Surgery Huashan HospitalCancer Metastasis InstituteFudan UniversityShanghai 200040China Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease School of Basic Medicine and Medical CenterUniversity of Science and Technology of ChinaHefei 230026China Department of Assisted Reproduction Shanghai Ninth People’s HospitalShanghai Jiao Tong University School of MedicineShanghai 200011China College of Pharmacy Ningxia Medical UniversityYinchuan 750004China Department of Pancreatic Surgery Shanghai General HospitalShanghai Key Laboratory of Pancreatic DiseaseInstitute of Pancreatic DiseaseShanghai Jiao Tong University School of MedicineShanghai 200080China

Pancreatic cancer,one of the most aggressive malignancies,has no effective treatment due to the lack of targets and drugs related to tumour ***6 can promote the migration of pancreatic cancer and could be a potential target for antimetastasis of pancreatic ***,highly selective and potency sirt6 inhibitor that can be used in vivo is yet to be ***,we developed a novesirt6 allosteric inhibitor,compound 11e,with maximal inhibitory potency and an IC_(50) value of 0.98±0.13μmol/***,compound 11e exhibited significant selectivity against other histone deacetylases(HADC1-11 and sirt1-3)at concentrations up to 100μmol/*** allosteric site and the molecular mechanism of inhibition were extensively elucidated by cocrystal complex structure and dynamic structural ***,we confirmed the antimetastatic function of such inhibitors in four pancreatic cancer cell lines as well as in two mouse models of pancreatic cancer liver *** our knowledge,this is the first study to reveal the in vivo effects of sirt6 inhibitors on liver metastatic pancreatic *** not only provides a promising lead compound for subsequent inhibitor developmentargeting sirt6 but also provides a potential approach to address the challenge of metastasis in pancreatic cancer.

关键词： sirt6 Inhibitor Allosteric Selectivity Cocrystal Pancreatic cancer metastasis

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Autophagy induction by sirt6 is involved in oxidative stress-induced neuronal damage

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Protein & Cell 2016年第4期7卷 281-290页

作者： Jiaxiang Shao Xiao Yang Tengyuan Liu Tingting Zhang Qian Reuben Xie Weiliang Xia State Key Laboratory of Oncogenes and Related Genes Renji-Med X Stem Cell Research Center Ren Ji Hospital School ofBiomedical Engineering Shanghai Jiao Tong University Shanghai 200030 China

sirt6 is a NAD＊-dependent histone deacetylase and has been implicated in the regulation of genomic stability, DNA repair, metabolic homeostasis and several diseases. The effect of sirt6 in cerebral ischemia and oxygen/glucose deprivation （OGD） has been reported, however the role of sirt6 in oxidative stress damage remains unclear. Here we used SH-SY5Y neuronal cells and found that overexpression of sirt6 led to decreased cell viability and increased necrotic cell death and reactive oxygen species （ROS） production under oxidative stress. Mechanistic study revealed that SlRT6 induced autophagy via attenuation of AKT signaling and treatment with autophagy inhibitor 3-MA or knockdown of autophagy-related protein Atg5 rescued HzO2-induced neuronal injury. Conversely, sirt6 inhibition suppressed autophagy and reduced oxidative stressinduced neuronal damage. These results suggest that sirt6 might be a potential therapeutic target for neuroprotection.

关键词： sirt6 oxidative stress neuronal damage,autophagy AKT

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Overexpression of sirt6 ameliorates sleep deprivation induced-cognitive impairment by modulating glutamatergic neuron function

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Neural Regeneration Research 2023年第11期18卷 2449-2458页

作者： Jinpiao Zhu Chang Chen Zhen Li Xiaodong Liu Jingang He Ziyue Zhao Mengying He Binbin Nie Zili Liu Yingying Chen Kuanpin Su Xiang Li Juxiang Chen Hongbing Xiang Fuqiang Xu Kangguang Lin Zongze Zhang Jie Wang Department of Anesthesiology Brain Research CenterDepartment of NeurosurgeryZhongnan HospitalWuhan UniversityWuhanHubei ProvinceChina Department of Anesthesiology and Pain Medicine Tongji Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina Department of Anesthesia and Intensive Care Peter Hung Pain Research InstituteThe Chinese University of Hong KongHong Kong Special Administration RegionChina Key Laboratory of Magnetic Resonance in Biological Systems State Key Laboratory of Magnetic Resonance and Atomic and Molecular PhysicsNational Center for Magnetic Resonance in WuhanWuhan Institute of Physics and MathematicsInnovation Academy for Precision Measurement Science and TechnologyChinese Academy of Sciences-Wuhan National Laboratory for OptoelectronicsWuhanHubei ProvinceChina Key Laboratory of Nuclear Radiation and Nuclear Energy Technology Institute of High Energy PhysicsChinese Academy of SciencesBeijingChina The Brain Cognition and Brain Disease Institute(BCBDI) NMPA Key Laboratory for Research and Evaluation of Viral Vector Technology in Cell and Gene Therapy Medicinal ProductsShenzhen Key Laboratory of Viral Vectors for BiomedicineShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research InstitutionsShenzhenGuangdong ProvinceChina Mind-Body Interface Research Center(MBI-Lab) China Medical University HospitalTaichungTaiwanChina An-Nan Hospital China Medical UniversityTainanTaiwanChina Department of Neurosurgery Changhai HospitalNaval Medical UniversityShanghaiChina Department of Affective Disorders The Affiliated Brain Hospital of Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Institute of Neuroscience and Brain Diseases Xiangyang Central HospitalAffiliated Hospital of Hubei University of Arts and ScienceXiangyangHubei ProvinceChina University of Chinese Academy of Sciences BeijingChina

Sleep benefits the restoration of energy metabolism and thereby suppo rts neuronal plasticity and cognitive ***6 is a NAD+-dependent protein deacetylase that has been recognized as an essential regulator of energy metabolism because it modulates various transcriptional regulators and metabolic *** aim of this study was to investigate the influence of sirt6 on cerebral function after chronic sleep deprivation(CSD).We assigned C57BL/6J mice to control or two CSD groups and subjected them to AAV2/9-CMV-EGFP or AAV2/9-CMV-sirt6-EGFP infection in the prelimbic cortex(PrL).We then assessed cerebral functional connectivity(FC) using resting-state functional MRI,neuron/astrocyte metabolism using a metabolic kinetics analysis;dendritic spine densities using sparse-labeling;and miniature excitato ry postsynaptic currents(mEPSCs) and action potential(AP) firing rates using whole-cell patchclamp *** addition,we evaluated cognition via a comprehensive set of behavioral *** with controls,sirt6 was significantly decreased(P6 ove rexpression reve rsed CSD-induced cognitive impairment and reduced *** analysis of metabolic kinetics using [1-13C] glucose and [2-13C] acetate showed that CSD reduced neuronal Glu4and GABA2synthesis,which could be fully restored via forced sirt6 ***,sirt6 ove rexpression reversed CSD-induced decreases in AP firing rates as well as the frequency and amplitude of mEPSCs in PrL pyramidal *** data indicate that sirt6 can improve cognitive impairment after CSD by regulating the PrL-associated FC network,neuronal glucose metabolism,and glutamatergic ***,sirt6 activation may have potential as a novel strategy for treating sleep disorder-related diseases.

关键词： chronic sleep deprivation cognitive impairment functional connectivity glutamatergic neurons metabolic kinetics neuronal-astrocytic glucose metabolism prelimbic cortex REM sleep sirt6 synaptic function

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Overexpressed sirt6 ameliorates doxorubicin-induced cardiotoxicity and potentiates the therapeutic efficacy through metabolic remodeling

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Acta Pharmaceutica Sinica B 2023年第6期13卷 2680-2700页

作者： Kezheng Peng Chenye Zeng Yuqi Gao Binliang Liu Liyuan Li Kang Xu Yuemiao Yin Ying Qiu Mingkui Zhang Fei Ma Zhao Wang The Ministry of Education Key Laboratory of Protein Science School of Pharmaceutical SciencesTsinghua UniversityBeijing 100084China Department of Medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China School of Medicine Tsinghua UniversityBeijing 100084China Department of Cardiac Surgery First Hospital of Tsinghua UniversityBeijing 100016China

Since the utilization of anthracyclines in cancer therapy, severe cardiotoxicity has become a major obstacle. The major challenge in treating cancer patients with anthracyclines is minimizing cardiotoxicity without compromising antitumor efficacy. Herein, histone deacetylase sirt6 expression was reduced in plasma of patients treated with anthracyclines-based chemotherapy regimens. Furthermore,overexpression of sirt6 alleviated doxorubicin-induced cytotoxicity in cardiomyocytes, and potentiated cytotoxicity of doxorubicin in multiple cancer cell lines. Moreover, sirt6 overexpression ameliorated doxorubicin-induced cardiotoxicity and potentiated antitumor efficacy of doxorubicin in mice, suggesting that sirt6 overexpression could be an adjunctive therapeutic strategy during doxorubicin ***, doxorubicin-impaired mitochondria led to decreased mitochondrial respiration and ATP production. And sirt6 enhanced mitochondrial biogenesis and mitophagy by deacetylating and inhibiting Sgk1. Thus, sirt6 overexpression coordinated metabolic remodeling from glycolysis to mitochondrial respiration during doxorubicin treatment, which was more conducive to cardiomyocyte metabolism, thus protecting cardiomyocytes but not cancer cells against doxorubicin-induced energy deficiency. In addition, ellagic acid, a natural compound that activates sirt6, alleviated doxorubicininduced cardiotoxicity and enhanced doxorubicin-mediated tumor regression in tumor-bearing *** findings provide a preclinical rationale for preventing cardiotoxicity by activating sirt6 in cancer patients undergoing chemotherapy, but also advancing the understanding of the crucial role of sirt6 in mitochondrial homeostasis.

关键词： sirt6 Doxorubicin Cardiotoxicity Antitumor efficacy Ellagic acid Mitochondrial homeostasis Glycolysis SGK1

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Hepatic sirt6 deficit promotes liver tumorigenesis in the mice models

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Genes & Diseases 2022年第3期9卷 789-796页

作者： Mei Wang Linhua Lan Fan Yang Shan Jiang Haojun Xu Chengfei Zhang Guoren Zhou Hongping Xia Jinglin Xia Department of Pathology in the School of Basic Medical Sciences&Sir Run Run Hospital&State Key Laboratory of Reproductive Medicine&Key Laboratory of Antibody Technique of National Health Commission Nanjing Medical UniversityNanjingJiangsu 211166PR China Department of Immunology Medical School of Southeast UniversityNanjingJiangsu 210009PR China The First Affiliated Hospital of Wenzhou Medical University WenzhouZhejiang 325000PR China The First Affiliated Hospital of Chongqing Medical University Chongqing 400016PR China Jiangsu Cancer Hospital&Jiangsu Institute of Cancer Research The Affiliated Cancer Hospital of Nanjing Medical UniversityNanjingJiangsu 210009PR China

sirt6 belongs to class III sirtuin family with NAD+-dependent histone deacetylase activities and controls multiple processes including aging,metabolism and *** recent years,increasing studies showed tumor suppressor role of sirt6 in HCC *** established a two-stage DEN followed CC14 induced liver carcinogenesis in the hepatic-specific sirt6 HKO mice models and found that hepatic S1RT6 deficit significantly promotes liver injury and liver cancer through inhibition of the ERK1/2 ***6 was compensatory up-regulated in mice tumor tissues and human HCC cells and overexpressed sirt6 inhibits tumor growth both in vitro and in *** together,we provide a useful mouse model for delineating the molecular pathways involved in chronic liver diseases and primary liver cancer and suggest that sirt6 can be a promising target for HCC therapies.

关键词： ERK1/2 pathway HCC Liver carcinogenesis Mouse model sirt6

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Overexpression of sirt6 prevents hypoxia-induced apoptosis in osteoblast cells

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中国药理学与毒理学杂志 2017年第5期31卷 482-483页

作者： WANG Jin-tao YIN Xi-ya GAO Shan ZHOU Lu Department of Sports Medicine Taishan Mecical University

OBJECTIVE To investigated the role of sirt6 in the survival of osteoblast cel s against hypoxia stimulus as wel as the underlying mechanism. METHODS MC3T3-E1 osteoblast cel s were used. Apoptosis was induced by hypoxic treatment. MC3T3-E1 cells were transfected with adenovirus sirt6. For sirt6 silencing experiment,the transfection of cells were done using three si RNA duplexes directed at different regions of sirt6 or scrambled siRNA pool. The relative levels of sirt6 mR NA were quantifiedby using real-time PCR. Western blotting experiments were done after the specific treatment and sample collection. MTT assay was used to estimate cell viability. Caspase 3/7 activity was assayed. RESULTS The expression of sirt6 mR NA appeared to be markedly down-regulated in the hypoxia-treated group compared to the matched normal group. Meanwhile,western blotting analysis revealed that the expression of sirt6 level was markedly down-regulated in hypoxia-treated group at protein level. sirt6 level was effectively down-regulated by the transfection of sirt6 si RNA,and significantly enhanced by sirt6 overexpression. Compared with the control group,sirt6 overexpression could significantly increase cell viability,and significantly decrease the percentage of apoptotic cel s and the activity of caspase 3/7 in response to hypoxia treatment. By contrast,sirt6 knockdown via treatment with sirt6 si RNA exhibited the opposite phenotype. CONCLUSION These results suggest that sirt6 plays a protective role in hypoxia-induced apoptosis in MC3T3-E1 cells,and that strategies might be beneficial for the treatment of ischemic bone disease.

关键词： sirt6 hypoxia apoptosis osteoblast

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sirt6/NF-κB信号轴在人参皂苷Rg_1延缓造血干/祖细胞衰老中的作用

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中国中药杂志 2015年第3期40卷 511-515页

作者：周玥唐艳隆王亚平王建伟丁继超大理学院组织学与胚胎学教研室云南大理671000 大理学院附属医院放射科云南大理671000 重庆医科大学干细胞与组织工程研究室组织学与胚胎学教研室重庆400016

目的:探讨sirt6/NF-κB信号轴在人参皂苷Rg1延缓造血干/祖细胞衰老中的作用,为寻找延缓HSC/HPC衰老途径提供理论和实验依据。方法:免疫磁性分选法分离纯化Sca-1+HSC/HPC后分为:正常对照组、衰老组、阳性对照组、Rg1延缓衰老组、Rg1治疗... 详细信息

目的:探讨sirt6/NF-κB信号轴在人参皂苷Rg1延缓造血干/祖细胞衰老中的作用,为寻找延缓HSC/HPC衰老途径提供理论和实验依据。方法:免疫磁性分选法分离纯化Sca-1+HSC/HPC后分为:正常对照组、衰老组、阳性对照组、Rg1延缓衰老组、Rg1治疗衰老组。衰老相关β-半乳糖苷酶(SA-β-Gal)细胞化学染色、流式细胞术分析细胞周期和造血祖细胞混合集落(CFU-Mix)培养确定Rg1延缓或治疗Sca-1+HSC/HPC衰老生物学作用。荧光定量PCR及Western blotting检测衰老调控分子sirt6,NF-κB mRNA及蛋白的表达。结果:与衰老组相比,Rg1延缓及治疗衰老组SA-β-gal染色阳性细胞百分比降低,G1期细胞比例下降,生成CFU-Mix数量增加,sirt6 mRNA及蛋白表达上调,NF-κB mRNA及蛋白表达下调;Rg1延缓衰老组各指标变化均较Rg1治疗衰老组明显。结论:Rg1可能通过调控sirt6-NF-κB信号通路发挥其对抗t-BHP诱导的Sca-1+HSC/HPC衰老的作用。

关键词：人参皂苷Rg1 sirt6 NF-κB Sca-1HSC/HPC 衰老

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