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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(Pc7,c-Myc and USP10 in tumors were significantly higher than the paired normal tissues from 148 EScc patients(Pcc patients with high HDAc7,c-Myc or USP10levels predicted worse overall survival(log-rank Pco-IP and Western blotting further revealed that HDAc7physically deacetylated and activated β-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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WSB1 regulates c-Myc expression through β-catenin signaling and forms a feedforward circuit

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1225-1239页

作者： Xiaomeng Gao Jieqiong You Yanling Gong Meng Yuan Haiying Zhu Liang Fang Hong Zhu Meidan Ying Qiaojun He Bo Yang Ji cao Institute of Pharmacology and Toxicology Zhejiang Province Key Laboratory of Anti-Cancer Drug ResearchCollege of Pharmaceutical SciencesZhejiang UniversityHangzhou 310058China The Innovation Institute for Artificial Intelligence in Medicine Zhejiang UniversityHangzhou 310058China Department of Biology Southern University of Science and TechnologyShenzhen 518055China cancer center of Zhejiang University Hangzhou 310058China

The dysregulation of transcription factors is widely associated with tumorigenesis.As the most well-defined transcription factor in multiple types of cancer,c-Myc can transform cells by transactivating various downstream genes.Given that there is no effective way to directly inhibit c-Myc,c-Myc targeting strategies hold great potential for cancer therapy.In this study,we found that WSB1,which has a highly positive correlation with c-Myc in 10 cancer cell lines and clinical samples,is a direct target gene of c-Myc,and can positively regulate c-Myc expression,which forms a feedforward circuit promoting cancer development.RNA sequencing results from Bel-7402 cells confirmed that WSB1 promoted cmyc expression through theβ-catenin pathway.Mechanistically,WSB1 affectedβ-catenin destruction complex-PPP2cA assembly and E3 ubiquitin ligase adaptorβ-TRcP recruitment,which inhibited the ubiquitination ofβ-catenin and transactivated c-Myc.Of interest,the effect of WSB1 on c-Myc was independent of its E3 ligase activity.Moreover,overexpressing WSB1 in the Bel-7402 xenograft model could further strengthen the tumor-driven effect of c-Myc overexpression.Thus,our findings revealed a novel mechanism involved in tumorigenesis in which the WSB1/c-Myc feedforward circuit played an essential role,highlighting a potential c-Myc intervention strategy in cancer treatment.

关键词： Transcription factors c-Myc WSB1 Ubiquitinationproteasome pathway β-catenin destruction complex Feedback loop Tumorigenesis cancer treatment

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Abemaciclib抑制c-Myc高表达小细胞肺癌增殖、侵袭和迁移的生物学功能的研究

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中国肺癌杂志 2023年第2期26卷 105-112页

作者：郭晶晶牟迪于文文孙蕾娜张家丽任秀宝韩颖天津医科大学肿瘤医院生物技术研究室国家恶性肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市恶性肿瘤临床医学研究中心天津市肿瘤免疫与生物治疗重点实验室天津300060 天津医科大学肿瘤医院病理科国家恶性肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市恶性肿瘤临床医学研究中心天津市肿瘤免疫与生物治疗重点实验室天津300060 天津医科大学肿瘤医院生物治疗科国家恶性肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市恶性肿瘤临床医学研究中心天津市肿瘤免疫与生物治疗重点实验室天津300060

背景与目的 c-Myc高表达小细胞肺癌(small cell lung cancer, ScLc)因易复发转移导致患者生存率极低,细胞周期依赖性激酶4和6(cyclin-dependent kinases 4 and 6, cDK4/6)抑制剂Abemaciclib在多种肿瘤的治疗中均起到关键作用,但其对ScL... 详细信息

背景与目的 c-Myc高表达小细胞肺癌(small cell lung cancer, ScLc)因易复发转移导致患者生存率极低,细胞周期依赖性激酶4和6(cyclin-dependent kinases 4 and 6, cDK4/6)抑制剂Abemaciclib在多种肿瘤的治疗中均起到关键作用,但其对ScLc的作用及机制仍不明晰。本研究旨在分析Abemaciclib抑制c-Myc高表达的ScLc增殖、侵袭和迁移的作用和分子机制,以期为减少患者的复发和转移拓展新的方向。方法通过STRING数据库分析了cDK4/6和c-Myc蛋白相互作用网络,免疫组化实验分析了31例ScLc癌组织和配对的相邻正常组织中cDK4/6及c-Myc的表达,ccK-8实验和平板克隆实验检测Abemaciclib对ScLc增殖的影响,Transwell及划痕实验检测Abemaciclib对ScLc的侵袭和迁移能力的影响,Western blot检测Abemaciclib对cDK4/6及相关转录因子的影响,流式细胞术分析了Abemaciclib对ScLc的细胞周期和免疫检查点的调节作用。结果通过STRING蛋白相互作用网络分析发现cDK4/6的表达均与c-Myc相关,c-Myc可以直接调节AScL1(achaete-scute complex homolog 1)、NEUROD1(neuronal differentiation 1)和Yes相关蛋白1(Yes-associated protein 1, YAP1)的表达,cDK4和c-Myc均调控程序性死亡配体1(programmed cell death ligand 1, PD-L1)的表达。通过免疫组化实验发现,cDK4/6及c-Myc在ScLc癌组织中的表达高于癌旁组织(PccK-8实验、平板克隆实验、Transwell实验及划痕实验验证了Abemaciclib可以有效地抑制SBc-2和H446OE的增殖、侵袭和迁移(Pciclib在抑制SBc-2和H446OE细胞内cDK4(PcDK6(Pc-Myc(PcL1(PcLc浸润和转移相关的蛋白。流式细胞术发现Abemaciclib不仅抑制ScLc的细胞周期进程(Pc-2(Pciclib明显抑制ScLc的增殖、侵袭、迁移和细胞周期进程,其通过抑制cDK4/6下调c-Myc、AScL1、YAP1和NEUROD1蛋白表达的同时,也提高了PD-L1的表达。

关键词：肺肿瘤细胞周期依赖性激酶4/6 c-Myc

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Overexpression of c-Myc-dependent heterogeneous nuclear ribonucleoprotein A1 promotes proliferation and inhibits apoptosis in NOTcH1-mutated chronic lymphocytic leukemia cells

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chinese Medical Journal 2022年第8期135卷 920-929页

作者： Yixin Zou Hanning Tang Yi Miao Huayuan Zhu Li Wang Lei Fan Jianxin Fu Wei Xu Jianyong Li Yi Xia department of Hematology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjingJiangsu 210029China Key Laboratory of Hematology of Nanjing Medical University NanjingJiangsu 210029China collaborative Innovation center for cancer Personalized Medicine NanjingJiangsu 210029China Pukou cLL center NanjingJiangsu 210000China

Background: NOTcH1 mutation is an essential molecular biologic aberration in chronic lymphocytic leukemia (cLL). cLL patients withNOTcH1 mutation have shown an unfavorable survival and a poor response to chemoimmunotherapy. This study aims to present the mechanisms of adverse prognosis caused byNOTcH1 mutation from the perspective of the splicing factor heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1).Methods: The microarray data in Gene Expression Omnibus datasets were analyzed by bioinformatics and the function of hnRNPA1 was checked by testing the proliferation and apoptosis of cLL-like cell lines. Afterward, quantitative reverse transcription-polymerase chain reaction and Western blotting were applied to explore the relationship among NOTcH1, c-Myc, and hnRNPA1.Results: RNA splicing was found to play a vital part inNOTcH1-mutated cLL cells;hence, hnRNPA1 was selected as the focus of this study. Higher expression of hnRNPA1 validated in primaryNOTcH1-mutated cLL samples could promote proliferation and inhibit apoptosis in cLL. The expression of hnRNPA1 increased when NOTcH1 signaling was activated by transfection with NOTcH1 intracellular domain (NIcD)-overexpressed adenovirus vector and declined after NOTcH1 signaling was inhibited by NOTcH1-shRNA. Higher expression of c-Myc was observed in NIcD-overexpressed cells and hnRNPA1 expression was downregulated after applying c-Myc inhibitor 10058-F4. Moreover, in NIcD-overexpressed cells, hnRNPA1 expression decreased through c-Myc inhibition.conclusion: Overexpression of c-Myc-dependent hnRNPA1 could promote proliferation and inhibit apoptosis inNOTcH1- mutated cLL cells, which might partly account for the poor prognosis of patients withNOTcH1 mutation.

关键词： chronic lymphocytic leukemia NOTcH1 mutation c-Myc Heterogeneous nuclear ribonucleoprotein A1

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PLEK2 promotes cancer stemness and tumorigenesis of head and neck squamous cell carcinoma via the c-Myc-mediated positive feedback loop

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cancer communications 2022年第10期42卷 987-1007页

作者： Xinyuan Zhao Dalong Shu Wenjuan Sun Shanshan Si Wei Ran Bing Guo Li cui Department of Endodontics Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Department of Oral and Maxillofacial Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Stomatology The Third Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510630P.R.China Department of Oral Emergency Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Department of Dentistry The First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Department of Oral and Maxillofacial Surgery Stomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280P.R.China Division of Oral Biology and Medicine School of DentistryUniversity of CaliforniaLos AngelesLos AngelesCalifornia 90095United States

Background:Head and neck squamous cell carcinoma(HNScc)is one of the most frequent malignancies worldwide and is characterized by unfavorable prognosis,high lymph node metastasis and early recurrence.However,the molecular events regulating HNScc tumorigenesis remain poorly understood.Therefore,uncovering the underlying mechanisms is urgently needed to identify novel and promising therapeutic targets for HNScc.In this study,we aimed to explore the role of pleckstrin-2(PLEK2)in regulating HNScc tumorigenesis.Methods:The expression pattern of PLEK2 and its clinical significance in HNScc were determined by analyzing publicly assessable datasets and our own independent HNScc cohort.In vitro and in vivo experiments,including cell proliferation,colony formation,Matrigel invasion,tumor sphere formation,ALDEFLUOR,Western blotting assays and xenograft mouse models,were used to investigate the role of PLEK2 in regulating the malignant behaviors of HNScc cells.The underlying molecular mechanisms for the tumor-promoting role of PLEK2 were elucidated using co-immunoprecipitation,cycloheximide chase analysis,ubiquitination assays,chromatin immunoprecipitation-quantitative polymerase chain reaction,luciferase reporter assays and rescue experiments.Results:The expression levels of PLEK2 mRNA and protein were significantly increased in HNScc tissues,and PLEK2 overexpression was strongly associated with poor overall survival and therapeutic resistance.Additionally,PLEK2 was important for maintaining the proliferation,invasion,epithelial-mesenchymal transition,cancer stemness and tumorigenesis of HNScc cells and could alter the cellular metabolism of the cancer cells.Mechanistically,PLEK2 interacted with c-Myc and reduced the association of F-box and WD repeat domain containing 7(FBXW7)with c-Myc,thereby avoiding ubiquitination and subsequent proteasome-mediated degradation of c-Myc.Moreover,the c-Myc signaling activated by PLEK2 was important for sustaining the aggressive malignant phenotypes and tumorigenesis of HNScc cells.c-M

关键词： c-Myc cancer stemness FBXW7 HNScc PLEK2 positive feedback loop tumorigenesis ubiquitination-mediated degradation

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c-Myc-mediated TRIB3/P62^(+) aggresomes accumulation triggers paraptosis upon the combination of everolimus and ginsenoside Rh2

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1240-1253页

作者： Min-Xia Su Yu-Lian Xu Xiao-Ming Jiang Mu-Yang Huang Le-Le Zhang Luo-Wei Yuan Xiao-Huang Xu Qi Zhu Jian-Li Gao Jia-Hong Lu Xiuping chen Ming-Qing Huang Yitao Wang Jin-Jian Lu State Key Laboratory of Quality Research in chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao 999078China School of Pharmaceutical Sciences Zhejiang Chinese Medical UniversityHangzhou 310000China college of Pharmacy Fujian University of Traditional Chinese MedicineFuzhou 350000China Mo E Frontiers Science center for Precision Oncology University of MacaoMacao 999078China

The mammalian target of rapamycin(m TOR) pathway is abnormally activated in lung cancer.However, the anti-lung cancer effect of m TOR inhibitors as monotherapy is modest. Here, we identified that ginsenoside Rh2, an active component of Panax ginseng c. A. Mey., enhanced the anti-cancer effect of the m TOR inhibitor everolimus both in vitro and in vivo. Moreover, ginsenoside Rh2 alleviated the hepatic fat accumulation caused by everolimus in xenograft nude mice models. The combination of everolimus and ginsenoside Rh2(labeled Eve-Rh2) induced caspase-independent cell death and cytoplasmic vacuolation in lung cancer cells, indicating that Eve-Rh2 prevented tumor progression by triggering paraptosis. EveRh2 up-regulated the expression of c-Myc in cancer cells as well as tumor tissues. The increased cmyc mediated the accumulation of tribbles homolog 3(TRIB3)/P62+ aggresomes and consequently triggered paraptosis, bypassing the classical c-Myc/MAX pathway. Our study offers a potential effective and safe strategy for the treatment of lung cancer. Moreover, we have identified a new mechanism of TRIB3/P62+ aggresomes-triggered paraptosis and revealed a unique function of c-Myc.

关键词： Everolimus Ginsenoside Rh2 Paraptosis Aggresomes P62 TRIB3 c-Myc Lung cancer

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Lin28B和c-Myc蛋白在喉鳞癌中的表达及其与临床病理特征和预后的相关性

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中南大学学报（医学版） 2023年第2期48卷 165-171页

作者：廖非非曹雨鑫黄美响初令王天生中南大学湘雅三医院病理科长沙410013 中南大学湘雅三医院耳鼻喉头颈外科长沙410013

目的:喉鳞癌是头颈部常见恶性肿瘤。将原癌基因与抑癌基因作为研究的突破口从而筛选恶性肿瘤治疗的靶基因是如今肿瘤研究焦点之一。寻找喉鳞癌治疗及预后相关的靶基因分子至关重要。本研究旨在检测Lin28B和c-Myc蛋白在喉鳞癌及其对应癌... 详细信息

目的:喉鳞癌是头颈部常见恶性肿瘤。将原癌基因与抑癌基因作为研究的突破口从而筛选恶性肿瘤治疗的靶基因是如今肿瘤研究焦点之一。寻找喉鳞癌治疗及预后相关的靶基因分子至关重要。本研究旨在检测Lin28B和c-Myc蛋白在喉鳞癌及其对应癌旁组织中的表达,初步探讨其与喉鳞癌临床病理特征及预后的关系。方法:采用免疫组织化学法检测102例喉鳞癌患者的癌组织及其对应的90例癌旁组织中Lin28B与c-Myc蛋白的表达情况,分析Lin28B与c-Myc蛋白在喉鳞癌中表达的相关性及其表达水平与喉鳞癌临床病理特征之间的关系。采用Kaplan-Meier法分析喉鳞癌患者术后生存率与Lin28B和c-Myc蛋白表达水平之间的关系。结果:与癌旁组织相比,Lin28B、cmyc蛋白的表达水平在喉鳞癌组织中均显著升高(均Pc-Myc蛋白的表达与喉鳞癌患者淋巴结转移情况、临床分期、肿瘤大小和病理分化程度密切相关(均Pc-Myc蛋白(Pc-Myc蛋白在喉鳞癌组织中高表达且呈正相关,两者均与患者的淋巴结转移情况、临床分期、肿瘤大小、病理分化程度及预后相关,提示Lin28B和c-Myc可能都参与喉鳞癌的发生、发展。

关键词： Lin28B c-Myc 喉鳞癌临床病理特征预后

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胡桃醌通过促进c-Myc泛素化降解抑制宫颈癌细胞的生长和促进凋亡

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南方医科大学学报 2022年第7期42卷 1026-1031页

作者：赵行宇杨昆宋梓桐何涵张巍吉林医药学院生化教研室吉林吉林132013 延边大学基础医学院生化教研室吉林延边133000

目的观察c-Myc蛋白在宫颈癌HeLa细胞中的表达,探讨胡桃醌通过影响c-Myc蛋白泛素化降解进而影响HeLa细胞的增殖与凋亡。方法培养人宫颈癌HeLa细胞,分为对照组:正常培养;10、20、50μmol/L胡桃醌组:培养液中分别加入对应浓度的胡桃醌。以W... 详细信息

目的观察c-Myc蛋白在宫颈癌HeLa细胞中的表达,探讨胡桃醌通过影响c-Myc蛋白泛素化降解进而影响HeLa细胞的增殖与凋亡。方法培养人宫颈癌HeLa细胞,分为对照组:正常培养;10、20、50μmol/L胡桃醌组:培养液中分别加入对应浓度的胡桃醌。以Westernblot方法分析胡桃醌处理后c-Myc蛋白的表达。HeLa细胞分为对照组和20μmol/L胡桃醌组,在培养0、2、4、8 h分别用Westernblot检测c-Myc蛋白表达的变化;放线菌酮(cHX)法检测c-Myc蛋白半衰期的变化;coIP方法检测c-Myc蛋白降解影响。HeLa细胞分为空白对照组:正常培养;胡桃醌组:20μmol/L胡桃醌培养液培养;0.5、1.0、2.0μmol/LMG132组:分别与0、1.0、2.0μmol/L蛋白酶体抑制剂MG132加20μmol/L胡桃醌培养,检测c-Myc蛋白表达的水平。将si c-Myc转染入HeLa细胞后,将细胞分siNc组:空载体组;si-Nc;胡桃醌组:空载体加20μmol/L胡桃醌处理;si-cmyc组:转染myc RNA;sicmyc20μmol/L胡桃醌组:转染myc RNA加20μmol/L胡桃醌处理。MTT及流式细胞术检测20μmol/L胡桃醌处理后对敲除及未敲除c-Myc基因的细胞增殖及凋亡的影响。结果与对照组相比,不同浓度胡桃醌可下调c-Myc蛋白表达且曾时间及剂量依赖性(Pc-Myc蛋白的半衰期,加入不同浓度的MG132后,即可明显上调c-Myc蛋白水平(Pc-Myc蛋白的泛素降解水平。未敲除c-Myc组相比,敲除组在胡桃醌处理后吸光度值明显增加(Pc-Myc蛋白的泛素化降解过程,进而抑制HeLa细胞增殖并促进其凋亡的发生。

关键词：胡桃醌宫颈癌 HeLa c-Myc 泛素化

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芍药苷抑制SENP1/c-Myc信号通路诱导急性B淋巴细胞白血病细胞的凋亡和周期阻滞

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中国中药杂志 2022年第12期47卷 3312-3319页

作者：覃祥陈曦刘静曾艳郭铃刘文君西南医科大学附属医院儿科儿童血液肿瘤与出生缺陷实验室四川泸州646000 四川省出生缺陷临床医学研究中心四川泸州646000

探讨芍药苷对人急性B淋巴细胞白血病(B-cell acute lymphoblastic leukemia,B-ALL)细胞凋亡、周期的影响及作用机制。体外培养Nalm-6和SUP-B15细胞,设对照组(0μg·mL^(-1))及芍药苷不同剂量组(200、400、800μg·mL^(-1))。细胞计数试... 详细信息

探讨芍药苷对人急性B淋巴细胞白血病(B-cell acute lymphoblastic leukemia,B-ALL)细胞凋亡、周期的影响及作用机制。体外培养Nalm-6和SUP-B15细胞,设对照组(0μg·mL^(-1))及芍药苷不同剂量组(200、400、800μg·mL^(-1))。细胞计数试剂盒(cell counting kit-8,ccK-8)检测Nalm-6和SUP-B15细胞活力;流式细胞术分析细胞凋亡和细胞周期分布;免疫印迹法检测活化的半胱氨酸蛋白酶-3(cleaved caspase-3)、活化的多聚腺苷二磷酸核糖聚合酶(cleaved poly ADP-ribose polymerase,cleaved PARP)、c-Myc和小泛素样修饰物特异性蛋白酶1(small ubiquitin-like modifier-specific protease 1,SENP1)蛋白的表达情况;基于Oncomine数据库分析急性淋巴细胞白血病(acute lymphoblastic leukemia,ALL)患者中c-Myc和SENP1基因mRNA的表达水平;采用AutoDock软件进行分子对接分析芍药苷与c-Myc和SENP1蛋白的相互作用关系。结果显示,芍药苷抑制Nalm-6和SUP-B15细胞活力,并呈浓度和时间依赖性;与对照组比较,芍药苷显著上调凋亡相关蛋白cleaved caspase-3、cleaved PARP的表达,诱导Nalm-6和SUP-B15细胞凋亡;显著增加Nalm-6和SUP-B15细胞G_(2)/M期细胞比例,诱导G_(2)/M期阻滞;显著下调Nalm-6和SUP-B15细胞c-Myc和SENP1蛋白的表达水平。ALL患者中c-Myc和SENP1基因mRNA表达水平较正常组显著增加。分子对接显示,芍药苷与c-Myc和SENP1蛋白均具有良好的结合作用。综上,芍药苷通过诱导细胞凋亡和G_(2)/M期阻滞抑制Nalm-6和SUP-B15细胞增殖,其机制可能与c-Myc和SENP1蛋白下调有关。

关键词：芍药苷急性B淋巴细胞白血病凋亡周期阻滞 c-Myc SENP1

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急性T淋巴细胞白血病的miR-211、miR-155、c-Myc表达水平及相关性研究

引用

中国实验血液学杂志 2022年第2期30卷 425-429页

作者：郑阳陈良郭树霞宋银森郑州人民医院转化医学研究中心河南郑州450000 郑州人民医院检验科河南郑州450000 郑州人民医院血液科河南郑州450000

目的:分析并探讨急性T淋巴细胞白血病(T-ALL)的miR-211、miR-155、c-Myc表达及相关性,旨在为早期诊断及预后监测提供依据。方法:选择2014年6月-2017年6月于郑州人民医院接受诊治的T-ALL患者96例,另选同期体检健康的志愿者69例为对照组,... 详细信息

目的:分析并探讨急性T淋巴细胞白血病(T-ALL)的miR-211、miR-155、c-Myc表达及相关性,旨在为早期诊断及预后监测提供依据。方法:选择2014年6月-2017年6月于郑州人民医院接受诊治的T-ALL患者96例,另选同期体检健康的志愿者69例为对照组,采用实时荧光定量PcR测定各组外周血单个核细胞中miR-211、miR-155、c-Myc表达水平,通过Kaplan-Meier分析T-ALL患者生存情况及miR-211、miR-155和c-Myc与预后的关系,Pearson相关分析评价miR-211、miR-155和c-Myc与疾病危险度的相关性。结果:T-ALL组miR-211 mRNA、miR-155 mRNA、c-Myc mRNA表达水平均明显高于对照组(Pc-Myc低表达患者生存时间亦明显长于高表达患者(Pc-Myc高表达与疾病高危呈线性正相关(r=0.749、0.781、0.804)。结论:T-ALL患者miR-211、miR-155、c-Myc表达上调,其表达水平与预后密切相关,且与疾病危险度呈线性正相关。

关键词：急性T淋巴细胞白血病 miR-211 miR-155 c-Myc 相关性

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