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miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer

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Journal of Molecular Cell Biology 2018年第4期10卷 302-315页

作者： sanhong liu Zifeng Wang Zukai liu Shuo Shi Zhaoran Zhang Jiawei Zhang Haifan Lin Shanghai Institute of Advanced Immunochemical Studies ShanghaiTech University Shanghai China School of Life Science and Technology ShanghaiTech University Shanghai China The Yale Stem Cell Center and Department of Cell Biology Yale University School of Medicine New Haven CT USA

Triple-negative breast cancer （TNBC）, characterized by the lack of expression of the estrogen receptor, the progesterone receptor, and the human epidermal growth factor receptor 2, is an aggressive form of cancer that conveys unpredictable and poor prognosis due to limited treatment options and lack of effective targeted therapies. Wnt/β-catenin signaling is hyperactivated in TNBC, which promotes the progression of TNBC. However, the molecular mechanism of Wnt/β-catenin activation in TNBC remains unknown. Here, we report the drastic overexpression of miR-221/222 in all of four TNBC cell lines and TNBC primary tumor samples from patients. Furthermore, we demonstrate by both ex vivo and xenograft experiments that inhibiting miR-221/222 expression in a TNBC cell line （MDA-MB-231） suppresses its proliferation, viability, epithelial-to-mesenchymal transition, and migration; whereas expressing miR-221/222 in a non-TNBC line （MCF7） promotes all of the above cancer properties. miR-221/222 achieve so by directly repressing multiple negative regulators of the Wnt/β-catenin signaling pathway, including WIF1, SFRP2, DKK2, and AXIN2, to activate the pathway. Notably, the level of miR-221/222 expression is inversely correlated whereas that of WIF1, DKK2, SFRP2, and AXIN2 expression is positively correlated with the patient survival. Last, we show that anti-miR-221/222 significantly increases apoptotic cells with tamoxifen/Wnt3a treatment but not with cyclophosphamide/Wnt3a treatment. These results demonstrate that miR-221/222 activate the Wnt/β-catenin signaling to promote the aggressiveness and TNBC properties of breast cancers, and thus reveal a new prospect for TNBC treatment.

关键词： miR-221/222 Wnt/β-catenin triple-negative breast cancer

Elevating H3K27me3 level sensitizes colorectal cancer to oxaliplatin

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Journal of Molecular Cell Biology 2020年第2期12卷 125-137页

作者： Qi Wang Xi Chen Yuhang Jiang sanhong liu Hanshao liu Xiaohua Sun Haohao Zhang Zhi liu Yu Tao Cuifeng Li Yiming Hu Dandan liu Deji Ye Yongzhong liu Mingliang Wang Xiaoren Zhang The Key Laboratory of Stem Cell Biology Shanghai Jiao Tong University School of Medicine&Shanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200025227 Chongqing South RoadShanghaiChina Affiliated Cancer Hospital&Institute Guangzhou Medical UniversityGuangzhou 510000195 Dongfeng West RoadGuangzhouChina Shanghai Institute for Advanced Immunochemical Studies ShanghaiTech UniversityShanghai 201210393 Huaxia Middle RoadShanghaiChina State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200032Ruijin 2nd RoadShanghaiChin Department of General Surgery Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025Ruijin 2nd RoadShanghaiChina

Histone methylation is a context-dependent modification that regulates gene expression,and the trimethylation of histone H3 lysine 27(H3K27me3)usually induces gene *** colorectal cancer(CRC)chemoresistance is currently a huge challenge,but the relationship between H3K27me3 modification and chemoresistance remains largely ***,we found that H3K27me3 levels positively correlated with the metastasis-free survival of CRC patients and a low H3K27me3 level predicted a poor outcome upon chemotherapeutic drug *** stimulation significantly induced the expression of H3K27 lysine demethylase 6A/6B(KDM6A/6B),thus decreasing the level of H3K27me3 in CRC *** of H3K27me3 level through KDM6A/6B depletion or GSK-J4(a KDM6A/6B inhibitor)treatment significantly enhanced oxaliplatin-induced ***,when inhibiting the expression of H3K27me3 by EPZ-6438,an inhibitor of the histone methyltransferase EZH2,the proportion of apoptotic cells remarkably *** addition,the combination of GSK-J4 and oxaliplatin significantly inhibited tumor growth in an oxaliplatin-resistant patient-derived xenograft ***,we revealed that oxaliplatin treatment dramatically induced NOTCH2 expression,which was caused by downregulation of H3K27me3 level on the NOTCH2 transcription initiation ***,the activated NOTCH signaling promoted the expression of stemness-related genes,which resulted in oxaliplatin ***,oxaliplatin-induced NOTCH signaling could be interrupted by GSK-J4 ***,our findings suggest that elevating H3K27me3 level can improve drug sensitivity in CRC patients.

关键词： H3K27 trim ethylation colorectal cancer chem oresistance NOTCH signaling

Bruceine D inhibits HIF-1α-mediated glucose metabolism in hepatocellular carcinoma by blocking ICAT/β-catenin interaction

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Acta Pharmaceutica Sinica B 2021年第11期11卷 3481-3492页

作者： Rui Huang Lijun Zhang Jinmei Jin Yudong Zhou Hongwei Zhang Chao Lv Dong Lu Ye Wu Hong Zhang sanhong liu Hongzhuan Chen Xin Luan Weidong Zhang Institute of Interdisciplinary Integrative Medicine Research Shanghai University of Traditional Chinese MedicineShanghai 201203China School of Pharmacy Second Military Medical UniversityShanghai 200433China Department of Chemistry and Biochemistry College of Liberal ArtsUniversity of MississippiUniversityMS 38677-1848USA

Hepatocellular carcinoma(HCC)is one of the leading causes of cancer-related deaths,characterized by highly hypoxic tumor ***-inducible factor-1α(HIF-1α)is a major regulator involved in cellular response to changes of oxygen levels,supporting the adaptation of tumor cells to *** D(BD)is an isolated natural quassinoid with multiple anti-cancer ***,we identified BD could significantly inhibit the HIF-1α expression and its subsequently mediated HCC cell *** biophysical proteomics approaches,we identified inhibitor of β-catenin and T-cell factor(ICAT)as the functional target of *** targeting ICAT,BD disrupted the interaction of bcatenin and ICAT,and promoted β-catenin degradation,which in turn induced the decrease of HIF-1α ***,BD could inhibit HCC cells proliferation and tumor growth in vivo,and knockdown of ICAT substantially increased resistance to BD treatment in *** data highlight the potential of BD as a modulator of β-catenin/HIF-1α axis mediated HCC metabolism.

关键词： Hepatocellular carcinoma Bruceine D HIF-1α Metabolism ICAT β-Catenin Tumor microenvironment Hypoxia

Bcl-3 promotes Wnt signaling by maintaining the acetylation ofβ-catenin at lysine 49 in colorectal cancer

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1913-1924页

作者： Xi Chen Chen Wang Yuhang Jiang Qi Wang Yu Tao Haohao Zhang Yongxu Zhao Yiming Hu Cuifeng Li Deji Ye Dandan liu Wenxia Jiang Eugene Y.Chin Sheng Chen Yongzhong liu Mingliang Wang sanhong liu Xiaoren Zhang CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesUniversity of Chinese Academy of SciencesChinese Academy of SciencesShanghai 200025China Shanghai Institute for Advanced Immunochemical Studies ShanghaiTech UniversityShanghai 201210China Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and DegradationState Key Laboratory of Respiratory DiseaseGuangzhou 510000China Renji Hospital Shanghai Jiao Tong University School of MedicineShanghai 200025China State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200032China Department of General Surgery Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Wnt/β-catenin signaling plays a critical role in colorectal cancer(CRC)tumorigenesis and the homeostasis of colorectal cancer stem cells(CSCs),but its molecular mechanism remains unclear.B-cell lymphoma 3(Bcl-3),a member of the IκB family,is overexpressed in CRC and promotes ***,we report a novel function of Bcl-3 in maintaining colorectal CSC homeostasis by activating Wnt/β-catenin *** Bcl-3 suppresses the self-renewal capacity of colorectal CSCs and sensitizes CRC cells to chemotherapeutic drugs through a decrease in Wnt/β-catenin ***,our data show that Bcl-3 is a crucial component of Wnt/β-catenin signaling and is essential forβ-catenin transcriptional activity in CRC ***,Wnt3a increases the level and nuclear translocation of Bcl-3,which binds directly toβ-catenin and enhances the acetylation ofβ-catenin at lysine 49(Ac-K49-β-catenin)and transcriptional ***-3 depletion decreases the Ac-K49-β-catenin level by increasing the level of histone deacetylase 1 to remove acetyl groups fromβ-catenin,thus interrupting Wnt/β-catenin *** CRC clinical specimens,Bcl-3 expression negatively correlates with the overall survival of CRC patients.A significantly positive correlation was found between the expression of Bcl-3 and Ac-K49-β-***,our data reveal that Bcl-3 plays a crucial role in CRC chemoresistance and colorectal CSC maintenance via its modulation of the Ac-K49-β-catenin,which serves as a promising therapeutic target for CRC.

关键词： colorectal homeostasis cancer

The histone H3 lysine-27 demethylase Jmjd3 plays a critical role in specific regulation of Th17 cell differentiation

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分子细胞生物学报:英文版 2015年第6期7卷 505-516页

作者： Zhi liu Wei Cao Longxia Xu Xi Chen Yu Zhan Qian Yang sanhong liu Pengfei Chen Yuhang Jiang Xiaohua Sun Yu Tao Yiming Hu Cuifeng Li Qi Wang Ying Wang Charlie Degui Chen Yufang Shi Xiaoren Zhang Key Laboratory of Stem Cell Biology Institute of Health SciencesShanghai Institutes for Biological SciencesChinese Academy of Sciences and Shanghai Jiao Tong University School of MedicineShanghai 200031China State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China Collaborative Innovation Center of Systems Biomedicine Shanghai Jiao Tong University School of MedicineShanghai 200240China

Interleukin(IL)17-producing T helper(Th17)cells play critical roles in the clearance of extracellular bacteria and fungi as well as the pathogenesis of various autoimmune diseases,such as multiple sclerosis,psoriasis,and ulcerative *** a global transcriptional regulatory network of Th17 cell differentiation has been mapped recently,the participation of epigenetic modifications in the differentiation process has yet to be *** demonstrated here that histone H3 lysine-27(H3K27)demethylation,predominantly mediated by the H3K27 demethylase Jmjd3,crucially regulated Th17 cell *** of naı¨ve CD41 T cells immediately induced high expression of *** depletion of Jmjd3 in CD41 T cells specifically impaired Th17 cell differentiation both in vitro and in *** expression of Jmjd3 largely rescued the impaired differentiation of Th17 cells in vitro in Jmjd3-deficientCD41 T ***,Jmjd3-deficient mice were resistant to the induction of experimental autoimmune encephalomyelitis(EAE).Furthermore,inhibition of the H3K27 demethylase activity with the specific inhibitor GSK-J4 dramatically suppressed Th17 cell differentiation in *** the molecular level,Jmjd3 directly bound to and reduced the level of H3K27 trimethylation(me3)at the genomic sites ofRorc,which encodes the masterTh17 transcription factorRorgt,and Th17 cytokine genes such as Il17,Il17f,and ***,our studies established acritical role of Jmjd3-mediatedH3K27demethylation inTh17 cell differentiation andsuggest that Jmjd3 can be a novel therapeutic target for suppressing autoimmune responses.

关键词： histone H3K27 demethylation Jmjd3 Th17 cells autoimmune disease

优化企业生态效率评价的生命周期评价(LCA)-物质流成本会计(MFCA)整合方法

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科技管理研究 2023年第16期43卷 70-78页

作者：刘三红梁雯张伟绍兴文理学院商学院浙江绍兴312000 杭州电子科技大学会计学院浙江杭州310018 绍兴文理学院元培学院浙江绍兴312000

为更客观、准确评价企业制造过程的生态效率水平,弥补现有文献未见考虑结合生命周期分析(LCA)和物质流成本会计(MFCA)评价方法的缺失,通过探讨LCA和MFCA之间的联系和区别,开发整合LCA和MFCA的企业生态效率评价方法。LCA-MFCA方法主要包... 详细信息

为更客观、准确评价企业制造过程的生态效率水平,弥补现有文献未见考虑结合生命周期分析(LCA)和物质流成本会计(MFCA)评价方法的缺失,通过探讨LCA和MFCA之间的联系和区别,开发整合LCA和MFCA的企业生态效率评价方法。LCA-MFCA方法主要包括3个步骤:采用物质平衡分析、MFCA、LCA量化企业有关物质和经济损失以及外部环境损害成本;通过帕累托法则原理和假设分析、实地采访和参考现有文献,识别企业经济活动每个流程或物量中心中对环境损害影响最大的因素,基于此提出改进方案;通过重新执行MFCA和LCA来验证所提建议的改进选项。将LCA-MFCA方法运用于A水泥生产企业生态效率评价,借鉴日本的环境损害综合系数表(LIME)计算其主要物量中心所产出废弃物的外部损害成本,认为生料制成中心、窑尾预分解中心和煤粉制备中心等急需进行改进,同时提出使用袋除尘器代替原来的电除尘器、以电石渣取代石灰石和安装低温余热系统等3种优化方案。经验证,LCA-MFCA评价方法可行,不仅能够给企业带来更多的利润,还能减少企业对不可再生资源的耗费,达到优化生态效率的目标。

关键词：企业生态效率评价生命周期评价物质流成本会计外部环境损害循环经济

融合与创新:传统会计中物质流成本会计的导入研究

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河南师范大学学报（哲学社会科学版） 2016年第6期43卷 123-128页

作者：刘三红肖序周志方中南大学商学院湖南长沙410083 绍兴文理学院浙江绍兴312000

随着ISO14051的公布与执行,物质流成本会计(MFCA)已经证明其在环境管理中的重要作用,在我国企业的现有会计系统中导入MFCA显得尤为重要。MFCA和传统会计存在一定的互通性,可以从基本概念结构、信息与数据基础、核算程序与方法、信息披... 详细信息

随着ISO14051的公布与执行,物质流成本会计(MFCA)已经证明其在环境管理中的重要作用,在我国企业的现有会计系统中导入MFCA显得尤为重要。MFCA和传统会计存在一定的互通性,可以从基本概念结构、信息与数据基础、核算程序与方法、信息披露与报告以及循环反馈与优化应用模式等五个方面实现MFCA和传统会计系统的融合与互通。将MFCA顺利导入传统会计系统,可以弥补传统会计不能兼顾环境和经济效益的缺陷,使物质流转过程中的损失"可视化",更好地为企业环境管理服务。

关键词：物质流成本会计(MFCA) 传统会计循环经济企业管理

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浅析智慧课堂在小学科学教学中的实践研究

天津教育 2021年第30期 77-78,81页

作者：刘三红甘肃省张掖市临泽县板桥镇中心小学

随着教育教学不断改革与发展,我国已经进入了现代化高科技阶段,现代化教学的功能越来越强大,在实际教学中发挥着重要作用,有助于教学质量和教学效果的有效提升。小学科学是一门综合性、应用性、实践性很强的学科,其涉及的知识非常广泛,... 详细信息

随着教育教学不断改革与发展,我国已经进入了现代化高科技阶段,现代化教学的功能越来越强大,在实际教学中发挥着重要作用,有助于教学质量和教学效果的有效提升。小学科学是一门综合性、应用性、实践性很强的学科,其涉及的知识非常广泛,与其他学科都有一定的联系。教育工作对于信息技术的运用也屡见不鲜,将信息技术运用于教育工作当中,同时包括智慧课堂教学,可以有效提高教学效率和质量,推动学生成绩的提升。

关键词：智慧课堂小学科学实践研究

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儿童手足口病的数学建模和计算机模拟

数学物理学报（A辑） 2018年第5期38卷 1032-1040页

作者：李华刘三红方奕乐张兴安华中师范大学数学与统计学学院武汉430079 西安市长安区第三中学西安710000 湖北科技学院数学与统计学院湖北咸宁437100 武昌首义学院机电与自动化学院武汉430064

手足口病(HFMD)是由肠道病毒引起的传染病,患者主要是少儿,由EV71和CoxA16病毒引起.该文建立了传染病SEIHRS模型,模拟了2012-2016年手足口病患病者的数据,估计了手足口病每年的基本再生数,给出了手足口病少儿疫苗的接种率,预测了2017年... 详细信息

手足口病(HFMD)是由肠道病毒引起的传染病,患者主要是少儿,由EV71和CoxA16病毒引起.该文建立了传染病SEIHRS模型,模拟了2012-2016年手足口病患病者的数据,估计了手足口病每年的基本再生数,给出了手足口病少儿疫苗的接种率,预测了2017年手足口病患病者的数目并提出了预防控制策略.该文的结果能为该疾病的预防与控制工作提供理论依据.

关键词：手足口病基本再生数数据模拟 EV71疫苗免疫接种率