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Oncogenic β-catenin-driven liver cancer is susceptible to methotrexate-mediated disruption of nucleotide synthesis

Chinese Medical Journal 2024年第2期137卷 181-189页

作者： Fangming Liu Yuting Wu Baohui Zhang Shuhui Yang Kezhuo Shang Jie Li Pengju Zhang Weiwei Deng Linlin Chen Liang Zheng Xiaochen Gai Hongbing Zhang Department of Physiology State Key Laboratory of Common Mechanism Research for Major DiseasesHaihe Laboratory of Cell EcosystemInstitute of Basic Medical Sciences and School of Basic MedicineChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100005China Department of Physiology Institute of Basic Medical Sciences and School of Basic MedicineGraduate School of Peking Union Medical CollegeChinese Academy of Medical SciencesBeijing100005China Department of Physiology School of Life ScienceChina Medical UniversityShenyangLiaoning 110122China School of Life Sciences Westlake UniversityHangzhouZhejiang 310024China Key Laboratory of Pediatric Hematology and Oncology Ministry of HealthInstitute of Pediatric Translational MedicineShanghai Children’s Medical CenterShanghai Jiao Tong School of MedicineShanghai 200127China

Background:Liver cancer is largely resistant to chemotherapy.This study aimed to identify the effective chemotherapeutics forβ-catenin-activated liver cancer which is caused by gain-of-function mutation of catenin beta 1(CTNNB1),the most frequently altered proto-oncogene in hepatic neoplasms.Methods:Constitutiveβ-catenin-activated mouse embryonic fibroblasts(MEFs)were established by deleting exon 3(β-catenin^(Δ(ex3)/+)),the most common mutation site in CTNNB1 gene.A screening of 12 widely used chemotherapy drugs was conducted for the ones that selectively inhibitedβ-catenin^(Δ(ex3)/+)but not for wild-type MEFs.Untargeted metabolomics was carried out to examine the alterations of metabolites in nucleotide synthesis.The efficacy and selectivity of methotrexate(MTX)onβ-catenin-activated human liver cancer cells were determined in vitro.Immuno-deficient nude mice subcutaneously inoculated withβ-catenin wild-type or mutant liver cancer cells and hepatitis B virus(HBV);β-catenin^(lox(ex3)/+)mice were used,respectively,to evaluate the efficacy of MTX in the treatment ofβ-catenin mutant liver cancer.Results:MTX was identified and validated as a preferential agent against the proliferation and tumor formation ofβ-catenin-activated cells.Boosted nucleotide synthesis was the major metabolic aberration inβ-catenin-active cells,and this alteration was also the target of MTX.Moreover,MTX abrogated hepatocarcinogenesis of HBV;β-catenin^(lox(ex3)/+)mice,which stimulated concurrent Ctnnb1-activated mutation and HBV infection in liver cancer.Conclusion:MTX is a promising chemotherapeutic agent forβ-catenin hyperactive liver cancer.Since repurposing MTX has the advantages of lower risk,shorter timelines,and less investment in drug discovery and development,a clinical trial is warranted to test its efficacy in the treatment ofβ-catenin mutant liver cancer.

关键词： Liver cancer β-catenin Methotrexate Nucleotide synthesis Chemotherapy

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β-catenin Deletion in Regional Neural Progenitors Leads to Congenital Hydrocephalus in Mice

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Neuroscience Bulletin 2022年第1期38卷 81-94页

作者： Lin Ma Yanhua Du Xiangjie Xu Hexi Feng Yi Hui Nan Li Guanyu Jiang Xiaoqing Zhang Xiaocui Li Ling Liu Translational Medical Center for Stem Cell Therapy Shanghai East HospitalSchool of MedicineTongji UniversityShanghai200120China Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of the Ministry of Education Orthopaedic Department of Tongji HospitalShanghai200065China Brain and Spinal Cord Innovative Research Center School of MedicineTongji UniversityShanghai200092China Key Laboratory of Neuroregeneration of Shanghai Universities School of MedicineTongji UniversityShanghai200092China Tsingtao Advanced Research Institute Tongji UniversityQingdao266071China Shanghai Institute of Stem Cell Research and Clinical Translation Shanghai200120China Department of Pathology and Pathophysiology School of MedicineTongji UniversityShanghai200092China Department of Immunology and Microbiology Shanghai Institute of ImmunologyShanghai Jiao Tong University School of MedicineShanghai200025China Shanghai First Maternity and Infant Hospital School of MedicineTongji UniversityShanghai200092China

Congenital hydrocephalus is a major neurological disorder with high rates of morbidity and mortality;however,the underlying cellular and molecular mechanisms remain largely unknown.Reproducible animal models mirroring both embryonic and postnatal hydrocephalus are also limited.Here,we describe a new mouse model of congenital hydrocephalus through knockout ofβ-catenin in Nkx2.1-expressing regional neural progenitors.Progressive ventriculomegaly and an enlarged brain were consistently observed in knockout mice from embryonic day 12.5 through to adulthood.Transcriptome profiling revealed severe dysfunctions in progenitor maintenance in the ventricular zone and therefore in cilium biogenesis afterβ-catenin knockout.Histological analyses also revealed an aberrant neuronal layout in both the ventral and dorsal telencephalon in hydrocephalic mice at both embryonic and postnatal stages.Thus,knockout ofβ-catenin in regional neural progenitors leads to congenital hydrocephalus and provides a reproducible animal model for studying pathological changes and developing therapeutic interventions for this devastating disease.

关键词： Congenital hydrocephalus β-catenin Ependymal cells Nkx2.1 Neural development

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Sijunzi Decoction Inhibits Stemness by Suppressingβ-catenin Transcriptional Activity in Gastric Cancer Cells

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Chinese Journal of Integrative Medicine 2022年第8期28卷 702-710页

作者： LI Yue-jun LIAO Lin-li LIU Pei TANG Ping WANG Hong PENG Qing-hua Department of Oncology the Third Affiliated Hospital of Hunan University of Chinese MedicineZhuzhou412000Hunan ProvinceChina Department of Oncology the First Affiliated Hospital of Hunan College of Traditional Chinese MedicineZhuzhou412000Hunan ProvinceChina Hunan Provincial Key Laboratory for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine Hunan University of Chinese MedicineChangsha410208China

Objective:To investigate a previously uncharacterized function of Sijunzi Decoction(SJZD)in inhibition of gastric cancer stem cells(GCSCs).Methods:MKN74 and MKN45,two CD44 positive gastric cancer cell lines with stem cell properties were used.The cells were divided into 2 groups.Treatment group was treated with SJZD(1-5 mg/mL)for indicated time(48 h-14 days).The control group was treated with equal volume of phosphate buffered saline.Cell Counting Assay Kit-8 were used to measure cell viability.Spheroid colony formation and GCSCs marker expression were performed to determine GCSCs stemness.Cell fractionation and chromatin immunoprecipitation assays were used to assess the distribution and DNA-binding activity of β-catenin after SJZD treatment,respectively.Results:SJZD treatment repressed cell growth and induced apoptosis in MKN74 and MKN45 cell lines(Pβ-catenin(Pβ-catenin.

关键词： Sijunzi Decoction Chinese medicine gastric cancer cancer stem cells β-catenin

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Melatonin inhibits ESCC tumor growth by mitigating the HDAC7/β-catenin/c-Myc positive feedback loop and suppressing the USP10-maintained HDAC7 protein stability

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Military Medical Research 2023年第2期10卷 207-226页

作者： Zhi-Qiang Ma Ying-Tong Feng Kai Guo Dong Liu Chang-Jian Shao Ming-Hong Pan Yi-Meng Zhang Yu-Xi Zhang Di Lu Di Huang Fan Zhang Jin-Liang Wang Bo Yang Jing Han Xiao-Long Yan Yi Hu Department of Medical Oncology Senior Department of Oncologythe Fifth Medical CenterChinese PLA General HospitalBeijing 100853China Department of Thoracic Surgery Tangdu Hospitalthe Fourth Military Medical UniversityXi’an 710038China Department of Cardiothoracic Surgery the 71th Group Army Hospital of PLAthe Affiliated Huaihai Hospital of Xuzhou Medical UniversityXuzhou 221004JiangsuChina Department of Thoracic Surgery Shaanxi Provincial People’s Hospitalthe Third Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710068China State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical SciencesPeking Union Medical CollegeBeijing 100037China Department of Ophthalmology Tangdu Hospitalthe Fourth Military Medical UniversityXi’an 710038China Department of Cardiovascular Surgery Xijing Hospitalthe Fourth Military Medical UniversityXi’an 710032China

Background:Melatonin,a natural hormone secreted by the pineal gland,has been reported to exhibit antitumor properties through diverse mechanisms of action.However,the oncostatic function of melatonin on esophageal squamous cell carcinoma(ESCC) remains elusive.This study was conducted to investigate the potential effect and underlying molecular mechanism of melatonin as single anticancer agent against ESCC cells.Methods:ESCC cell lines treated with or without melatonin were used in this study.In vitro colony formation and 5-Ethynyl-2’-deoxyuridine(EdU) incorporation assays,and nude mice tumor xenograft model were used to confirm the proliferative capacities of ESCC cells.RNA-seq,qPCR,Western blotting,recombinant lentivirus-mediated target gene overexpression or knockdown,plasmids transfection and co-IP were applied to investigate the underlying molecular mechanism by which melatonin inhibited ESCC cell growth.IHC staining on ESCC tissue microarray and further survival analyses were performed to explore the relationship between target genes’ expression and prognosis of ESCC.Results:Melatonin treatment dose-dependently inhibited the proliferative ability and the expression of histone deacetylase 7(HDAC7),c-Myc and ubiquitin-specific peptidase 10(USP10) in ESCC cells(Pβ-catenin thus promoting downstream target c-Myc gene transcription.Notably,our mechanistic study validated that HDAC7/β-catenin/c-Myc could form the positive feedback loop to enhance ESCC cell growth,and USP10 could deubiquitinate and stabilize HDAC7 protein in the ESCC cells.Additionally,we verified that inhibition of the HDAC7/β-catenin/c-Myc axis and USP10/HDAC

关键词： Melatonin Histone deacetylase 7(HDAC7) β-catenin c-Myc Ubiquitin-specifc peptidase 10(USP10) Esophageal squamous cell carcinoma(ESCC)

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TRIM21可抑制肝癌细胞的侵袭能力:基于泛素化途径降解β-catenin

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南方医科大学学报 2022年第1期42卷 55-62页

作者：张志红朱真如盛海龙孙景苑曹传辉南方医科大学南方医院放疗科广东广州510515

目的探讨TRIM21基因在肝癌侵袭表型中的作用及机制。方法利用siRNA敲低肝癌细胞MHCC 97H,HCC LM3中的TRIM21、β-catenin基因,将肝癌细胞分为对照组:转染对照siRNA;TRIM21敲低组:转染siTRIM21 RNA;CTNNB1敲低组:转染siCTNNB1 RNA;双敲低... 详细信息

目的探讨TRIM21基因在肝癌侵袭表型中的作用及机制。方法利用siRNA敲低肝癌细胞MHCC 97H,HCC LM3中的TRIM21、β-catenin基因,将肝癌细胞分为对照组:转染对照siRNA;TRIM21敲低组:转染siTRIM21 RNA;CTNNB1敲低组:转染siCTNNB1 RNA;双敲低组:共转染siTRIM21 RNA及siCTNNB1 RNA。利用Western blotting验证敲除效率及相关通路的激活或抑制情况。通过Transwell侵袭实验检测肿瘤细胞的侵袭性。通过尾静脉注射敲低TRIM21的HCC LM3细胞构建裸鼠肺转移模型以观测其肺转移能力。在HEK 293细胞中过表达TRIM21,将HEK 293细胞分为对照组:加入转染试剂;过表达组:转染flagTRIM21。并利用Co-IP检测TRIM21蛋白与β-catenin的相互作用及泛素化水平。生信分析TCGA数据库中CTNNB1^(high)TRIM21^(high)和CTNNB1^(high)TRIM21^(low)两种亚型肝癌的预后。结果敲低TRIM21可以显著增强肝癌细胞MHCC 97H和HCC LM3的侵袭能力(Pβ-catenin以减少其入核,进而降低肝癌细胞的的侵袭性(Pβ-catenin来抑制肝癌细胞的侵袭性,这可能导致了CTNNB1^(high)TRIM21^(low)肝癌患者预后较差。

关键词：肝癌侵袭性 TRIM21 β-catenin 泛素化预后

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SDCBP-AS1 destabilizesβ-catenin by regulating ubiquitination and SUMOylation of hnRNP K to suppress gastric tumorigenicity and metastasis

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Cancer Communications 2022年第11期42卷 1141-1161页

作者： Jing Han Menglin Nie Cong Chen Xiaojing Cheng Ting Guo Longtao Huangfu Xiaomei Li Hong Du Xiaofang Xing Jiafu Ji Department of Gastrointestinal Cancer Translational Research Laboratory Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer HospitalBeijing Institute for Cancer ResearchBeijing 100142P.R.China Department of Radiation Oncology Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070P.R.China Department of Gastrointestinal Surgery Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer HospitalBeijing Institute for Cancer ResearchBeijing 100142P.R.China

Background:Gastric cancer(GC)is among the most malignant tumors,yet the pathogenesis is not fully understood,especially the lack of detailed information about the mechanisms underlying long non-coding RNA(lncRNA)-mediated post-translational modifications.Here,the molecular mechanisms and clinical significance of the novel lncRNA syndecan-binding protein 2-antisense RNA 1(SDCBP2-AS1)in the tumorigenesis and progression of GC were investigated.Methods:The expression levels of SDCBP2-AS1 in 132 pairs of GC and adjacent normal tissues were compared,and the biological functions were assessed in vitro and in vivo.RNA pull-down and immunoprecipitation assays were conducted to clarify the interactions of SDCBP2-AS1 and heterogeneous nuclear ribonucleoprotein(hnRNP)K.RNA-sequencing,immunoprecipitation,immunofluorescence,and luciferase analyses were performed to investigate the functions of SDCBP2-AS1.Results:SDCBP2-AS1 was significantly downregulated in GC tissues and pre-dictive of poor patient prognosis.Silencing of SDCBP2-AS1 promoted the proliferation and migration of GC cells both in vitro and in vivo.Mechanically,SDCBP2-AS1 physically bound to hnRNP K to repress SUMOylation of hnRNP K and facilitated ubiquitination of hnRNP K andβ-catenin,thereby promoting the degradation ofβ-catenin in the cytoplasm.Silencing of SDCBP2-AS1 caused SUMOylation of hnRNP K and stabilizedβ-catenin activity,which altered tran-scription of downstream genes,resulting in tumorigenesis and metastasis of GC.Moreover,the knockdown of hnRNP K partially abrogated the effects of SDCBP2-AS1.Conclusions:SDCBP2-AS1 interacts with hnRNP K to suppress tumorigenesis and metastasis of GC and regulates post-transcriptional modifications of hnRNP K to destabilizeβ-catenin.These findings suggest SDCBP2-AS1 as a potential target for the treatment of GC.

关键词： SDCBP2-AS1 gastric cancer hnRNP K β-catenin post-transcriptional modifications tumori-genesis

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机械敏感离子通道Piezo1通过激活β-catenin诱导心房成纤维细胞衰老

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中国药理学通报 2023年第7期39卷 1234-1241页

作者：叶兴东罗雪珊李巧巧何锦涛徐玉雯杨慧邓春玉邝素娟张梦珍吴书林饶芳薛玉梅广东省心血管病研究所广东省人民医院广东省医学科学院广东广州510080

目的衰老心房成纤维细胞中新型机械敏感离子通道Piezo1的基因表达明显升高,观察其是否通过激活β-catenin参与心房成纤维细胞的衰老进程。方法通过酶消化法分离培养3~4周龄雄性C57BL/6小鼠原代心房成纤维细胞,给予叔丁基过氧化氢(TBHP... 详细信息

目的衰老心房成纤维细胞中新型机械敏感离子通道Piezo1的基因表达明显升高,观察其是否通过激活β-catenin参与心房成纤维细胞的衰老进程。方法通过酶消化法分离培养3~4周龄雄性C57BL/6小鼠原代心房成纤维细胞,给予叔丁基过氧化氢(TBHP)刺激建立衰老模型,检测衰老相关β-半乳糖苷酶(SA-β-Gal)活性。Western blot检测TBHP(100μmol·L^(-1))处理的细胞中Piezo1、β-catenin/p-β-catenin及衰老相关蛋白p53和p21的表达水平。衰老的小鼠心房成纤维细胞(MAFs)分别给予Piezo1通道抑制剂GsMTx4(3、10μmol·L^(-1))或Piezo1 siRNA,以及β-catenin抑制剂XAV939(3、10μmol·L^(-1));年轻的MAFs给予Piezo1特异性激动剂Yoda1(1、10μmol·L^(-1)),观察对细胞中β-catenin和衰老相关蛋白表达和活性的影响。结果 TBHP处理后,MAFs的SA-β-Gal染色阳性率明显增加,提示细胞发生衰老;且细胞中Piezo1、β-catenin/p-β-catenin和p53/p21的蛋白表达明显增加(Pβ-catenin(XAV939),可明显降低TBHP诱导的MAFs衰老率,以及减少β-catenin/p-β-catenin,p53/p21等蛋白表达和活性的增加(Pβ-catenin活性和衰老相关蛋白表达升高(Pβ-catenin诱导心房成纤维细胞衰老的病理过程。

关键词： Piezo1 β-catenin 心房成纤维细胞衰老心房颤动结构重构

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六味地黄汤对UUO大鼠肾组织β-catenin及EMT的影响

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中国药理学通报 2023年第12期39卷 2385-2389页

作者：王晖张海英高海波郭金晶裴刚唐群湖南中医药大学医学院湖南长沙410208 湖南中医药大学药学院湖南长沙410208

目的探讨六味地黄汤(Liuwei Dihuang decoction,LWDHD)对单侧输尿管梗阻(unilateral ureteric obstrutction,UUO)大鼠肾组织中上皮钙黏蛋白E(E-cadherin)、β-连环蛋白(β-catenin)、α-平滑肌肌动蛋白(α-SMA)的表达、肾脏组织病理变化及上皮-间质转化(epithelial-mesenchymal transformation,EMT)的影响。方法SPF级SD大鼠48只随机分成假手术组(Sham)、模型组(UUO)、LWDHD低、中、高组(LWDHD 3.375、6.75、13.5 g·kg^(-1))、依那普利组(Enalapril)10 mg·kg^(-1),每组8只。采用HE、Masson染色法观察6组大鼠患侧肾组织的病理变化和胶原纤维沉积情况;免疫组化及Western blot检测各组大鼠肾组织中上E-cadherin、β-catenin、α-SMA蛋白的表达情况。结果与Sham组比较,UUO组大鼠患侧肾组织中肾小球硬化,肾小管扩张,间质纤维化明显。β-catenin、α-SMA蛋白表达增加,E-cadherin蛋白表达降低(Pβ-catenin、α-SMA蛋白表达降低,E-cadherin蛋白表达增加(Pβ-catenin的表达,进而抑制EMT,发挥缓解肾纤维化的作用。

关键词：肾纤维化单侧输尿管梗阻 β-catenin EMT 六味地黄汤组织病理

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Semaphorin 7A promotes human vascular smooth muscle cell proliferation and migration through theβ-catenin signaling pathway

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BIOCELL 2023年第4期47卷 849-858页

作者： XIAOSU SONG FEN GAO HONG LI WEIWEI QIN CHANJUAN CHAI GUOJUAN SHI HUIYU YANG Department of Cardiology The Second Hospital of Shanxi Medical UniversityTaiyuan030001China

Background:Vascular smooth muscle cells(VSMCs)undergo a conversion from a contractile phenotype to a proliferative synthetic phenotype,contributing to the pathogenesis of cardiovascular diseases.Semaphorin 7A(SEMA7A)is a glycosylphosphatidylinositol-anchored membrane protein that plays an important role in vascular homeostasis by regulating endothelial cell behaviors.However,the expression and role of SEMA7A in VSMCs remain unclear.Methods:In this study,we screened for VSMC-regulating genes in publicly available datasets and analyzed the expression of SEMA7A in human coronary artery smooth muscle cells(hCASMCs)treated with platelet-derived growth factor-BB(PDGF-BB).The effects of SEMA7A overexpression and knockdown on hCASMC proliferation and migration were examined.The signaling pathways involved in the action of SEMA7A in hCASMCs were determined.Results:Bioinformatic analysis showed that SEMA7A was significantly dysregulated in VSMCs treated with oxidized low-density lipoprotein or overexpressing progerin,a pro-atherogenic gene.The PDGF-BB stimulation led to a concentration-and time-dependent induction of SEMA7A.Depletion of SEMA7A attenuated PDGF-BB-induced hCASMC proliferation and migration.Conversely,overexpression of SEMA7A enhanced hCASMC proliferation and migration.Mechanistically,SEMA7A stimulated the activation of theβ-catenin pathway and upregulated c-Myc,CCND1,and MMP7.Knockdown ofβ-catenin impaired SEMA7A-induced hCASMC proliferation and migration.Conclusions:SEMA7A triggers phenotype switching in VSMCs through theβ-catenin signaling pathway and may serve as a potential therapeutic target for cardiovascular diseases.

关键词： SEMA7A Vascular smooth muscle cell Phenotype switching Remodeling β-catenin

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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 microenvironment.Hypoxia-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 hypoxia.Bruceine D(BD)is an isolated natural quassinoid with multiple anti-cancer effects.Here,we identified BD could significantly inhibit the HIF-1α expression and its subsequently mediated HCC cell metabolism.Using biophysical proteomics approaches,we identified inhibitor of β-catenin and T-cell factor(ICAT)as the functional target of BD.By targeting ICAT,BD disrupted the interaction of bcatenin and ICAT,and promoted β-catenin degradation,which in turn induced the decrease of HIF-1α expression.Furthermore,BD could inhibit HCC cells proliferation and tumor growth in vivo,and knockdown of ICAT substantially increased resistance to BD treatment in vitro.Our 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

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