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Threonine 32 （Thr32） of foxo3 is critical for TGF-β-induced apoptosis via Bim in hepatocarcinoma cells

Protein & Cell 2015年第2期6卷 127-138页

作者： Xiangxuan Zhao Yong Liu Lei Du Leya He Biyun Ni Junbo Hu Dahai Zhu Quan Chen The Joint Laboratory of Apoptosis and Cancer Biology The State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China University of Chinese Academy of Sciences Beijing 100049 China Department of Radiology Shengjing Hospital of China Medical University Shenyang 110004 China Cancer Research Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430032 China Institute of Basic Medical Sciences of Chinese Academy of Medical Sciences and School of Basic Medicine of Peking Union Medical College Beijing 100005 China College of Life Science Nankai University Tianjin 300071 China

Transforming growth factor-β （TGF-β） exerts apoptotic effects on various types of malignant ceils, including liver cancer cells. However, the precise mechanisms by which TGF-β induces apoptosis remain poorly known. In the present study, we have showed that threonine 32 （Thr32） residue of foxo3 is critical for TGF-β to induce apoptosis via Bim in hepatocarcinoma Hep3B cells. Our data demonstrated that TGF-βinduced foxo3 activation through specific de-phosphorylation at Thr32. TGF-β-activated foxo3 cooperated with Smad2/ 3 to mediate Bim up-regulation and apoptosis. foxo3 （de）phosphorylation at Thr32 was regulated by casein kinase I-ε （CKI-E）. CKI inhibition by small molecule D4476 could abrogate TGF-β-induced foxo/Smad acti- vation, reverse Bim up-regulation, and block the sequential apoptosis. More importantly, the deregulated levels of CKI-ε and p32foxo3 were found in human malignant liver tissues. Taken together, our findings suggest that there might be a CKI-foxo/Smad-Bim engine in which Thr32 of foxo3 is pivotal for TGF-β- induced apoptosis, making it a potential therapeutic target for liver cancer treatment.

关键词： apoptosis TGF-β foxo3 casein kinasel-ε hepatocarcinoma

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foxo3 mutation predicting gefitinib-induced hepatotoxicity in NSCLC patients through regulation of autophagy

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Acta Pharmaceutica Sinica B 2022年第9期12卷 3639-3649页

作者： Shaoxing Guan Xi Chen Youhao Chen Guohui Wan Qibiao Su Heng Liang Yunpeng Yang Wenfeng Fang Yan Huang Hongyun Zhao Wei Zhuang Shu Liu Fei Wang Wei Feng Xiaoxu Zhang Min Huang Xueding Wang Li Zhang Laboratory of Drug Metabolism and Pharmacokinetics School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510060China State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China College of Health Science Guangdong Pharmaceutical UniversityGuangzhou 510006China Sun Yat-sen Memorial Hospital Sun Yat-sen UniversityGuangzhou 510080China Ersha Department of Pharmacy the Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou 510105China

Hepatotoxicity is a common side effect for patients treated with gefitinib,but the related pathogenesis is unclear and lacks effective predictor and management strategies.A multi-omics approach integrating pharmacometabolomics,pharmacokinetics and pharmacogenomics was employed in non-small cell lung cancer patients to identify the effective predictor for gefitinib-induced hepatotoxicity and explore optional therapy ***,we found that patients with rs4946935 AA,located in Forkhead Box O3(foxo3)which is a well-known autophagic regulator,had a higher risk of hepatotoxicity than those with the GA or GG variant(OR=18.020,95%CI=2.473 to 459.1784,P=0.018)in a gefitinib-concentration dependent ***,functional experiments identified that rs4946935_A impaired the expression of foxo3 by inhibiting the promotor activity,increasing the threshold of autophagy initiation and inhibiting the autophagic activity which contributed to gefitinib-induced liver *** contrast,erlotinib-induced liver injury was independent on the variant and expression levels of *** study reveals that foxo3 mutation,leading to autophagic imbalance,plays important role in gefitinib-induced hepatotoxicity,especially for patients with high concentration of *** conclusion,foxo3 mutation is an effective predictor and erlotinib might be an appropriately and well-tolerated treatment option for patients carrying rs4946935 AA.

关键词： Gefitinib Hepatotoxicity Pharmacometabolomic Pharmacokinetics Pharmacogenomics foxo3 Autophagy

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Neuroprotective mechanisms ofε-viniferin in a rotenone-induced cell model of Parkinson's disease:significance of SIRT3-mediated foxo3 deacetylation

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Neural Regeneration Research 2020年第11期15卷 2143-2153页

作者： Shuo Zhang Yan Ma Juan Feng Department of Neurology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Ultrasound Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Trans-(-)-ε-viniferin(ε-viniferin)has antioxidative and anti-inflammatory *** also has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway;however,it remains unknown whetherε-viniferin also has a neuroprotective role in Parkinson's disease.A Parkinson's disease cell model was induced by exposing SH-SY5 Y cells to 3.0μM rotenone for 24 hours,and cells were then treated with 1.0μMε-viniferin for 24 *** withε-viniferin upregulated SIRT3 expression,which promoted foxo3 deacetylation and nuclear localization.ε-Viniferin also increased ATP production and decreased reactive oxygen species ***,ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis,and restored the expression of mitochondrial homeostasis-related ***,when cells were transfected with SIRT3 or foxo3 shRNA prior to rotenone andε-viniferin treatment,these changes were *** results from the present study indicate thatε-viniferin enhances SIRT3-mediated foxo3 deacetylation,reduces oxidative stress,and maintains mitochondrial homeostasis,thus inhibiting rotenone-induced cell apoptosis.ε-Viniferin may therefore be a promising treatment strategy for Parkinson's disease.

关键词： deacetylation foxo3 mitochondrial homeostasis mitophagy oxidative stress Parkinson's disease SIRT3 ε-viniferin

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Single-nucleus profiling unveils a geroprotective role of the foxo3 in primate skeletal muscle aging

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Protein & Cell 2023年第7期14卷 499-514页

作者： Ying Jing Yuesheng Zuo Yang Yu Liang Sun Zhengrong Yu Shuai Ma Qian Zhao Guoqiang Sun Huifang Hu Jingyi Li Daoyuan Huang Lixiao Liu Jiaming Li Zijuan Xin Haoyan Huang Juan Carlos Izpisua Belmonte Weiqi Zhang Si Wang Jing Qu Guang-Hui Liu State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China University of Chinese Academy of Sciences Beijing 100049China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China China National Center for Bioinformation Beijing 100101China Aging Translational Medicine Center Intemational Center for Aging and CancerBeijing Municipal Geriatric Medical Research CenterXuanwu HospitalCapital Medical UniversityBeijing 100053China Department of Obstetrics and Gynecology Center for Reproductive MedicinePeking University Third HospitalBeijing 100191China The Key Laboratory of Geriatrics Beijing Institute of GeriatricsInstitute of Geriatric MedicineChinese Academy of Medical SciencesBeijing Hospital/National Center of Gerontology of National Health CommissionBeijing 100730China Clinical Stem Cell Research Center Peking University Third HospitalBeijing 100191China Department of Orthopaedics Peking University First HospitalBeijing 100034China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China Sino-Danish Center for Education and Research Beijing 101408China Altos Labs Inc.San DiegoCA 94022USA The Fifth People's Hospital of Chongqing Chongqing 400062China

Age-dependent loss of skeletal muscle mass and function is a feature of sarcopenia,and increases the risk of many aging-related metabolic ***,we report phenotypic and single-nucleus transcriptomic analyses of non-human primate skeletal muscle aging.A higher transcriptional fluctuation was observed in myonuclei relative to other interstitial cell types,indicating a higher susceptibility of skeletal muscle fiber to *** found a downregulation of foxo3 in aged primate skeletal muscle,and identi-fied foxo3 as a hub transcription factor maintaining skeletal muscle *** the establishment of a complementary experimental pipeline based on a human pluripotent stem cell-derived myotube model,we revealed that silence of foxo3 accelerates human myotube senescence,whereas genetic activation of endogenous foxo3 alleviates human myotube ***,based on a combination of monkey skeletal muscle and human myotube aging research models,we unraveled the pivotal role of the foxo3 in safeguarding primate skeletal muscle from aging,providing a comprehensive resource for the development of clinical diagnosis and targeted therapeutic interventions against human skeletal muscle aging and the onset of sarcopenia along with aging-relateddisorders.

关键词： single-nucleus RNA sequencing primate aging skeletal muscle foxo3

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MicroRNA-184 promotes proliferation ability of glioma cells by regulating foxo3

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Asian Pacific Journal of Tropical Medicine 2014年第10期7卷 776-779页

作者： Qing-Ke Cui Wei-Dong Liu Jian-Xin Zhu Yun-Hua Wang Zhi-Gang Wang Department of Neurosurgery The Qilu Hospital of Shandong University Liaocheng People's Hospital

Objective:To investigate the effect of microRNA(miR-184)on regulating the *** and prolifration of glioma ***:Lipidosome was used to transfect miR-184 mimic and inhibitor to glioma cell ling,and the cell proliferation ability changes were determined by MTT and plate cloning experiment after the *** test was used to measure the levels of cyclinD1,p27 and *** was used to detect miR-184expression in glioma cell *** tissues and adjacent *** experiment was used to test 3'UTR gene targeting regulation of miR-184 and ***:QPCR results showed a significaat lower miR-184 expression level in glioma cell line and glioma tissues than that in juxtacancerous *** and plate cloning experiments have shown that after overexpressing of miR-184,the cell proliferation capacity of glioma U87 and T98G was signifieantly increased,which was significantly inhibited after the inhibition of *** results showed a lower expression level of p27 in U87 and T98G cells,and a higher expression level of cyclind1after over-expressing of miR-184 wss ***.a lower expression level of eyelinD1and a higher expression level of p27 after the inhibition of *** luciferase activity was inhibited after the over-expressing of ***:MiR-184 can affect the proliferation abilities of glioma cells and regulate the cell cycle related *** plays an important role in the occurrence and development of gliomas.

关键词： miR-184 Glioma Cell proliferation foxo3

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miR-3682-3p directly targets foxo3 and stimulates tumor stemness in hepatocellular carcinoma via a positive feedback loop involving foxo3/PI3K/AKT/c-Myc

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World Journal of Stem Cells 2022年第7期14卷 539-555页

作者： Qian Chen Si-Bo Yang Ye-Wei Zhang Si-Yuan Han Lei Jia Bo Li Yi Zhang Shi Zuo Department of Hepatobiliary Surgery Affiliated Hospital of Guizhou Medical UniversityGuiyang 550000Guizhou ProvinceChina Department of Clinical Medicine Guizhou Medical UniversityGuiyang 550000Guizhou ProvinceChina Department of Infectious Diseases SSL Central Hospital of DongguanDongguan 523000Guangdong ProvinceChina Department of Organ Transplantation Affiliated Hospital of Guizhou Medical UniversityGuiyang 550000Guizhou ProvinceChina Department of Hepatobiliary Surgery Guizhou Provincial People's HospitalGuiyang 550000Guizhou ProvinceChina

BACKGROUND Cancer stem cells(CSCs) have been implicated in tumorigenesis and tumor recurrence and metastasis are key therapeutic targets in cancer *** display therapeutic potential by controlling the properties of CSCs;however, whether an association exists between miR-3682-3p and CSCs is *** To investigate the mechanism by which miR-3682-3p promotes stemness maintenance in hepatocellular carcinoma(HCC).METHODS MiR-3682-3p expression in HCC cell lines and 34 pairs of normal and HCC specimens was assayed by quantitative polymerase chain reaction. The functional role of miR-3682-3p was investigated in vitro and in vivo. Dual-luciferase reporter and chromatin immunoprecipitation assays were performed for target assessment, and western blotting was utilized to confirm miR-3682-3p/target *** We found that miR-3682-3p plays a key role in HCC pathogenesis by promoting HCC cell stemness. The upregulation of miR-3682-3p enhanced CSC spheroid-forming ability, side population cell fractions, and the expression of CSC factors in HCC cells in vitro and the tumorigenicity of transplanted HCC cells in vivo. Furthermore, silencing miR-3682-3p prolonged the survival of HCC-bearing mice. Mechanistically, we found that miR-3682-3p targets foxo3 and enables foxo3/β-catenin interaction, which promotes c-Myc expression through PI3K/AKT;cMyc, in turn, activates miR-3682-3p, forming a positive feedback loop. Intriguingly, miR-3682-3p expression was induced by hepatitis B virus X protein(HBx) and was involved in HBx-induced tumor stemness-related *** Our findings reveal a novel mechanism by which miR-3682-3p promotes stemness in HCC stem cells. Silencing miR-3682-3p may represent a novel therapeutic strategy for HCC.

关键词： miR-3682-3p foxo3 Cancer stem cells Hepatocellular carcinoma

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mTOR/Akt/foxo3信号通路在人参皂苷Rg_1抗PC-12细胞OGD损伤的作用

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中国中药杂志 2015年第8期40卷 1554-1559页

作者：严洁萍沈浓儿叶强宗永辉方晴霞吕良忠浙江省人民医院药学部浙江杭州310014

目的:研究人参皂苷Rg_1对PC-12细胞缺氧缺糖(oxygen-glucose deprivation,OGD)损伤的保护作用,并初步探讨与mTOR/Akt调控foxo3核浆穿梭相关的可能的分子机制。方法:建立OGD损伤PC-12细胞模型,MTT法检测OGD对PC-12细胞存活率。人参皂苷Rg... 详细信息

目的:研究人参皂苷Rg_1对PC-12细胞缺氧缺糖(oxygen-glucose deprivation,OGD)损伤的保护作用,并初步探讨与mTOR/Akt调控foxo3核浆穿梭相关的可能的分子机制。方法:建立OGD损伤PC-12细胞模型,MTT法检测OGD对PC-12细胞存活率。人参皂苷Rg_110,20,40μmol·L^(-1)预处理PC-12细胞24 h,加OGD损伤,MTT检测细胞存活率,比色法检测乳酸脱氢酶(LDH)释放、超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量。Western blot法检测mTOR,p-Akt^(ser473),p-Akt^(thr308),Akt,p-foxo3,细胞核、细胞质foxo3和总foxo3蛋白表达。结果:OGD作用4~24 h显著抑制PC-12细胞增殖,呈时间依赖性。Rg_1(20,40μmol·L^(-1))预处理24 h可显著增加细胞存活率,减少LDH释放,增加SOD活力和降低MDA含量。Rg_1可抑制由OGD引起的mTOR,p-Akt^(ser473)表达降低。OGD 6 h可减少foxo3磷酸化,并促进细胞质foxo3进入细胞核;预处理Rg_1增加foxo3磷酸化,促进foxo3进入细胞质。提示Rg_1可经由调控mTOR/Akt/foxo3信号通路抑制PC-12细胞损伤。结论:人参皂苷Rg_1可抑制OGD引起PC-12细胞损伤,作用机制可能与激活mTOR/Akt信号通路调控foxo3核质穿梭密切相关。

关键词： PC-12细胞人参皂苷Rg1 Akt磷酸化 mTOR foxo3 缺氧缺糖

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中耳胆脂瘤中P-Akt和foxo3的表达及其和凋亡的关系

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中华耳科学杂志 2021年第2期19卷 279-284页

作者：刘东亮马秀岚中国医科大学附属盛京医院耳鼻咽喉科耳科病房沈阳110004

目的检测人类叉头框O3(forkhead box O3,foxo3)蛋白、磷酸化蛋白激酶B(phosphorylated protein kinase B,P-Akt)在中耳胆脂瘤的表达和DAPI核染色情况。方法应用免疫荧光技术(immunofluorescence,IF)检测中国医科大学附属盛京医院2019年8月-11月期间30例中耳胆脂瘤标本(分为原发性胆脂瘤组和继发性胆脂瘤组)及15例正常皮肤标本中foxo3和DAPI核染色情况;应用Western blot免疫印迹法检测以上标本中P-Akt(ser473)、foxo3及内参GAPDH的表达情况;应用SPSS 22.0统计软件进行统计学分析。结果①免疫荧光实验显示,foxo3定位于胆脂瘤和正常皮肤的细胞核和细胞质,DAPI染色于细胞核;foxo3在中耳胆脂瘤的荧光值明显弱于正常皮肤,差异具有统计学意义(t=2.78,P=0.007,P3,Pfoxo3和DAPI在原发性胆脂瘤和继发性胆脂瘤的染色均无统计学差异。②Western blot免疫印迹法检测显示:胆脂瘤中P-Akt(ser473)的表达量明显高于正常皮肤中的表达量,两者差异具有统计学意义(t=2.05,P=0.02,Pfoxo3的表达量明显低于正常皮肤,差异具有统计学意义(t=1.94,P=0.04,Pfoxo3和DAPI呈显著正相关(r=0.451,P=0.001,P3)和foxo3的表达呈显著负相关(r=-0.466,P=0.0007,Pfoxo3荧光染色均弱于正常皮肤组织,且两者呈正相关;胆脂瘤中P-Akt表达明确高于正常皮肤组织,而foxo3在胆脂瘤中的表达明确低于正常皮肤,且两者呈负相关。这提示PI3K/Akt/foxo3通路通过抑制凋亡的方式参与中耳胆脂瘤的发病过程。

关键词：中耳胆脂瘤 foxo3 P-Akt DAPI

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伊马替尼耐药K562/G的microRNA表达谱分析及与foxo3/Bcl-6信号通路关系的研究

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中国实验血液学杂志 2022年第1期30卷 107-112页

作者：沈晶王欢王晶石魏娜王昭首都医科大学附属北京友谊医院血液内科北京100050

目的:探讨CML耐药细胞株K562/G耐药相关的foxo3/Bcl-6信号通路及相关microRNA(miRNA)机制。方法:采用MTT法检测伊马替尼对K562/G的耐药性;采用Western blot法检测耐药株和敏感株细胞中foxo3和Bcl-6蛋白的表达情况,实时荧光定量PCR检测FO... 详细信息

目的:探讨CML耐药细胞株K562/G耐药相关的foxo3/Bcl-6信号通路及相关microRNA(miRNA)机制。方法:采用MTT法检测伊马替尼对K562/G的耐药性;采用Western blot法检测耐药株和敏感株细胞中foxo3和Bcl-6蛋白的表达情况,实时荧光定量PCR检测foxo3及Bcl-6 mRNA的表达。运用miRNA芯片技术筛查K562与K562/G细胞之间差异表达的miRNA,进一步筛选foxo3/Bcl-6信号通路的靶向miRNA。结果:K562/G较K562细胞株的foxo3及Bcl-6蛋白表达均明显升高(Pfoxo3 mRNA表达明显升高(P3p、miR-4763-5p、miR-4664-5p和miR-3176与该信号通路相关。结论:伊马替尼耐药与foxo3/Bcl-6信号通路相关,并且K562/G与K562细胞存在miRNA表达显著差异。

关键词：慢性髓系白血病耐药 miRNA foxo3 Bcl-6

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foxo3和转录因子SOHLH1对卵母细胞特异性表达基因Bmp15转录活性的调控

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中国医科大学学报 2020年第7期49卷 628-635页

作者：刘源杜冰张雪金美玉郑志红中国医科大学实验动物部沈阳110122

目的探究foxo3和SOHLH1对卵母细胞特异性表达基因Bmp15的调控机制。方法构建foxo3-pcDNA3.0表达质粒、Bmp15-p GL3.0荧光质粒,用细胞免疫荧光实验验证这2种表达质粒在HEK293T细胞中的表达情况,双荧光素酶报告基因实验检测foxo3和转录因... 详细信息

目的探究foxo3和SOHLH1对卵母细胞特异性表达基因Bmp15的调控机制。方法构建foxo3-pcDNA3.0表达质粒、Bmp15-p GL3.0荧光质粒,用细胞免疫荧光实验验证这2种表达质粒在HEK293T细胞中的表达情况,双荧光素酶报告基因实验检测foxo3和转录因子SOHLH1对Bmp15启动子区的转录活性的影响,染色质免疫共沉淀实验验证foxo3和转录因子SOHLH1在Bmp15启动子区的结合情况。结果 foxo3-pcDNA3.0表达质粒、Bmp15-p GL3.0荧光质粒构建成功。foxo3-pcDNA3.0、Sohlh1-pcDNA3.0质粒成功转染HEK293T细胞并表达于其细胞核、质中。SOHLH1对Bmp15启动子(-2 000 bp,+200 bp)区域有正调控作用,该作用可被foxo3抑制,且呈剂量依赖性。SOHLH1蛋白能与Bmp15启动子(-170 bp,80 bp),(-450 bp,-220 bp),(-745bp,-560 bp),(-1 410 bp,-1 200 bp)区间结合。foxo3能与Bmp15启动子(120 bp,183 bp),(-84 bp,-75 bp),(-442bp,-395 bp),(-546 bp,-470 bp),(-674 bp,-665 bp)区间结合。结论 foxo3能抑制转录因子SOHLH1对卵母细胞特异性表达基因Bmp15的转录活性。

关键词：卵泡信号交流 SOHLH1 foxo3 Bmp15

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