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Long non-coding RNA colon cancer-associated transcript 1-Vimentin axis promoting the migration and invasion of HeLa cells

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中华医学杂志（英文版） 2023年第19期136卷 2351-2361页

作者： Zhangfu Li Jiangbei Yuan Qingen Da Zilong Yan Jianhua Qu Dan Li Xu Liu Qimin Zhan Jikui Liu China 518036 China Department of Cardiovascular Surgery Peking University Shenzhen Hospital Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen Guangdong 518036 China518036 China 518036 China 100021 China Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing) Laboratory of Molecular Oncology Peking University Cancer Hospital & Institute Beijing 100142 China100021

Background: Long non-coding RNA colon cancer-associated transcript 1 (CCAT1) is involved in transforming multiple cancers into malignant cancer types. Previous studies underlining the mechanisms of the functions of CCAT1 primarily focused on its decoy for miRNAs (micro RNAs). However, the regulatory mechanism of CCAT1–protein interaction associated with tumor metastasis is still largely unknown. The present study aimed to identify proteome-wide CCAT1 partners and explored the CCAT1–protein interaction mediated tumor metastasis. Methods: CCAT1–proteins complexes were purified and identified using RNA antisense purification coupled with the mass spectrometry (RAP-MS) method. The database for annotation, visualization, and integrated discovery and database for eukaryotic RNA binding proteins (EuRBPDB) websites were used to bioinformatic analyzing CCAT1 binding proteins. RNA pull-down and RNA immunoprecipitation were used to validate CCAT1–Vimentin interaction. Transwell assay was used to evaluate the migration and invasion abilities of HeLa cells. Results: RAP-MS method worked well by culturing cells with nucleoside analog 4-thiouridine, and cross-linking was performed using 365 nm wavelength ultraviolet. There were 631 proteins identified, out of which about 60% were RNA binding proteins recorded by the EuRBPDB database. Vimentin was one of the CCAT1 binding proteins and participated in the tumor metastasis pathway. Knocked down vimetin ( VIM ) and rescued the downregulation by overexpressing CCAT1 demonstrated that CCAT1 could enhance tumor migration and invasion abilities by stabilizing Vimentin protein. Conclusion: CCAT1 may bind with and stabilize Vimentin protein, thus enhancing cancer cell migration and invasion abilities.

关键词： lncRNA CCAT1 RAP-MS RNA binding protein Vimentin Migration Invasion

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Vimentin as a potential target for diverse nervous system diseases

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Neural Regeneration Research 2023年第5期18卷 969-975页

作者： Kang-Zhen Chen Shu-Xian Liu Yan-Wei Li Tao He Jie Zhao Tao Wang Xian-Xiu Qiu Hong-Fu Wu Department of Anesthesiology Guangzhou Huadu Hospital Affiliated to Guangdong Medical University(Guangzhou Huadu District Maternal and Child Health Care Hospital)GuangzhouGuangdong ProvinceChina Dongguan City Key Laboratory of Stem Cell and Regenerative Tissue Engineering Guangdong Medical UniversityDongguanGuangdong ProvinceChina Department of Surgery the Third Hospital of Guangdong Medical University(Longjiang Hospital of Shunde District)FoshanGuangdong ProvinceChina

Vimentin is a major type Ⅲ intermediate filament protein that plays important roles in several basic cellular functions including cell migration, proliferation, and division. Although Vimentin is a cytoplasmic protein, it also exists in the extracellular matrix and at the cell surface. Previous studies have shown that Vimentin may exert multiple physiological effects in different nervous system injuries and diseases. For example, the studies of Vimentin in spinal cord injury and stroke mainly focus on the formation of reactive astrocytes. Reduced glial scar, increased axonal regeneration, and improved motor function have been noted after spinal cord injury in Vimentin and glial fibrillary acidic protein knockout(GFAPVIM) mice. However, attenuated glial scar formation in post-stroke in GFAP–/– VIM–/– mice resulted in abnormal neuronal network restoration and worse neurological recovery. These opposite results have been attributed to the multiple roles of glial scar in different temporal and spatial conditions. In addition, extracellular Vimentin may be a neurotrophic factor that promotes axonal extension by interaction with the insulin-like growth factor 1 receptor. In the pathogenesis of bacterial meningitis, cell surface Vimentin is a meningitis facilitator, acting as a receptor of multiple pathogenic bacteria, including E. coli K1, Listeria monocytogenes, and group B streptococcus. Compared with wild type mice, VIMmice are less susceptible to bacterial infection and exhibit a reduced inflammatory response, suggesting that Vimentin is necessary to induce the pathogenesis of meningitis. Recently published literature showed that Vimentin serves as a double-edged sword in the nervous system, regulating axonal regrowth, myelination, apoptosis, and neuroinflammation. This review aims to provide an overview of Vimentin in spinal cord injury, stroke, bacterial meningitis, gliomas, and peripheral nerve injury and to discuss the potential therapeutic methods involving Vimentin manipulation in improving axonal regeneratio

关键词： astrocytes axonal regeneration bacterial meningitis glial scar gliomas nervous system diseases peripheral nervous system injury spinal cord injury stroke Vimentin

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低强度脉冲聚焦超声上调Vimentin蛋白表达抑制软骨细胞凋亡

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陆军军医大学学报 2023年第12期45卷 1292-1300页

作者：李东倩叶海霞虞乐华贾朗重庆医科大学附属第二医院康复医学科重庆400010 重庆城市管理职业学院康复教研室重庆401331

目的探讨低强度脉冲聚焦超声(focused low-intensity pulsed ultrasound,FLIPUS)通过机械效应抑制软骨细胞凋亡的分子机制。方法用胰蛋白酶联合Ⅱ型胶原酶提取C57BL/6J乳鼠膝关节原代软骨细胞进行体外实验,IL-1β处理细胞模拟骨关节炎... 详细信息

目的探讨低强度脉冲聚焦超声(focused low-intensity pulsed ultrasound,FLIPUS)通过机械效应抑制软骨细胞凋亡的分子机制。方法用胰蛋白酶联合Ⅱ型胶原酶提取C57BL/6J乳鼠膝关节原代软骨细胞进行体外实验,IL-1β处理细胞模拟骨关节炎样软骨细胞损伤并进行验证,同时检测不同处理时间下相关蛋白表达变化。细胞分为Control组、IL-1β组和IL-1β+FLIPUS组,流式细胞术检测各组软骨细胞凋亡率,细胞免疫荧光检测各组细胞中Vimentin的结构分布。Western blot检测各组Col2α1、MMP13、Bcl-2、Vimentin及p-Tyr397表达。结果提取软骨细胞并模拟了骨关节炎样软骨细胞损伤模型。与Control组相比,随着IL-1β处理时间的延长,Col2α1、Vimentin、p-Tyr397、Bcl-2和p-AKT蛋白表达降低(PVimentin及p-Tyr397表达上升(PVimentin排列分布发生重塑,荧光强度增加。结论FLIPUS上调软骨细胞Vimentin表达,促进FAK的Tyr397位点磷酸化,抑制软骨细胞凋亡。

关键词：低强度脉冲聚焦超声膝骨关节炎软骨细胞凋亡机械转导 Vimentin FAK

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miR-141-3p通过促进波形蛋白表达增强CNE-2人鼻咽癌细胞的增殖、侵袭和迁移

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细胞与分子免疫学杂志 2023年第1期39卷 63-69页

作者：孙哲周兰柱吴俊王文忠蚌埠医学院第一附属医院耳鼻喉科安徽蚌埠233000

目的探讨微小RNA 141-3p(miR-141-3p)能否通过调节波形蛋白(Vimentin)促进CNE-2人鼻咽癌(NPC)细胞的迁移。方法实时定量PCR检测NPC组织和癌旁组织miR-141-3p表达,免疫组织化学染色法和Western blot法检测Vimentin的表达水平。采用实时定... 详细信息

目的探讨微小RNA 141-3p(miR-141-3p)能否通过调节波形蛋白(Vimentin)促进CNE-2人鼻咽癌(NPC)细胞的迁移。方法实时定量PCR检测NPC组织和癌旁组织miR-141-3p表达,免疫组织化学染色法和Western blot法检测Vimentin的表达水平。采用实时定量PCR和Western blot法分别筛选5-8F、CNE-2、HNE1人NPC细胞中miR-141-3p相对表达量最高的细胞株,实时定量PCR和Western blot法共同验证miR-141-3p与Vimentin表达关系;采用小干涉RNA(si-miR-141-3p)下调CNE-2细胞miR-141-3p、噻唑蓝(MTT)法检测细胞增殖抑制率、Transwell^(TM)小室法检测细胞侵袭和迁移、Western blot法检测Vimentin表达量。结果与癌旁组织相比,NPC组织中miR-141-3p和Vimentin表达量均显著增加,与NP69细胞相比,miR-141-3p和Vimentin在CNE-2细胞中表达均显著增加;下调CNE-2细胞中miR-141-3p后,细胞侵袭和迁移能力均下降,细胞增殖能力显著降低,Vimentin蛋白表达量显著降低。结论miR-141-3p能够通过促进Vimentin表达增强CNE-2细胞的增殖和迁移。

关键词：鼻咽癌 miR-141-3p 上皮间质转化(EMT) Vimentin 细胞侵袭细胞迁移

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EGFR/Vimentin/Folic Acid磁球检测肺癌循环肿瘤细胞初探

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中国肺癌杂志 2020年第5期23卷 351-359页

作者：李国雷王赟谭国梁刘远徐曌冯浩兴伟徐志峰河北省中医院外一科石家庄050051 河北医科大学第三医院超声医学科石家庄050051

背景与目的循环肿瘤细胞(circulating tumor cell, CTC)在肺癌的筛查及预后方面发挥着重要的作用,但较低的CTC分离效率和特异性对其临床应用有着明显的制约,本研究旨在探讨非小细胞肺癌(non-small cell lung cancer, NSCLC)患者CTC的新... 详细信息

背景与目的循环肿瘤细胞(circulating tumor cell, CTC)在肺癌的筛查及预后方面发挥着重要的作用,但较低的CTC分离效率和特异性对其临床应用有着明显的制约,本研究旨在探讨非小细胞肺癌(non-small cell lung cancer, NSCLC)患者CTC的新型高效分离方法,以期达到对NSCLC的早期诊断的目的。方法采用薄膜法制备表皮生长因子受体(epidermal growth factor receptor, EGFR)、波形蛋白(Vimentin)和叶酸(folic acid, FA)三种免疫脂质磁球,表征后通过细胞系进行分选方案的探索,构建对NSCLC CTC的最优分选方案,初步研究了其在临床上的应用价值。结果 EGFR、Vimentin和FA磁球磁球单独和联合使用对肺癌细胞株的平均捕获效率分别为78.0%、79.0%、82.0%和91.0%;在60例肺癌患者中,以每7.5 mL血液2个CTC为cutoff值,EGFR、Vimentin、FA磁球单独和联合使用阳性率分别为65.0%、33.3%、93.3%和100.0%,同时发现联合使用三种磁球检出的CTC数量与临床分期具有相关性(PVimentin+和FA+表达且形态完整的CTC,有利于的CTC相关下游分析,本研究提供了一种提高NSCLC CTC捕获效率的新方法,且验证了捕获的CTC计数方法可用于肺癌的辅助诊断。

关键词：肺肿瘤循环肿瘤细胞 EGFR Vimentin 叶酸免疫磁球

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Vimentin modulates apoptosis and inflammatory cytokine release by a human monocytic cell line (THP-1) in response to lipopolysaccharides in vitro

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Chinese Medical Journal 2019年第11期132卷 1336-1343页

作者： Long-Xiang Su Pan Pan Xiao-Ting Wang Yu Long Da-Wei Liu Xiang Zhou Department of Critical Care Medicine Peking Union Medical College Hospital Peking Union Medical College Chinese Academy of Medical Sciences Beijing 100730 China Department of Critical Care Medicine Beijing Tiantan Hospital Capital Medical University Beijing 100070 China

Background:It has recently been recognized that serum Vimentin is elevated in infectious diseases,and that Vimentin plays a role in regulating neutrophils and macrophages associated inflammation.However,the mechanisms are unclear.This study was designed to explore the role of Vimentin in regulating monocyte survival or apoptosis as well as inflammatory cytokine secretion in response to lipopolysaccharides (LPSs).Methods:A human monocytic leukemia cell line (THP-1) was transfected with Vimentin-specific small interfering RNA (siRNA) or Vimentin over-expressing plasmid.Apoptosis was assessed by TdT-mediated dUTP Nick-End Labeling (TUNEL) and DNA content assay.Immunoblotting was performed to detect apoptosis-associated proteins.Cytokines (interleukin [IL]-6,IL-10,and tumor necrosis factor α [TNF-α]) were measured by enzyme-linked immuno sorbent assay.Two-way analysis of variance followed by Student's t test was used to compare means between different groups.Results:Suppression of Vimentin in THP-1 cells resulted in increased apoptotic response in the presence of LPS,while overexpression of Vimentin could prevent the cells from apoptosis in response to LPS.LPS alone or suppression of Vimentin resulted in significant up-regulation of caspase-3 (1.42 ± 0.20 of LPS alone and 1.68 ± 0.10 of Vimentin suppression vs.control,t =5.21 and 10.28,respectively,P Vimentin (140.9 ± 17.2 pg/day/105 cells vs.undetectable in control cells).Contusions:In summary,the Vimentin may regulate innate immunity through modulating monocytes viability as well as inflammatory response in sepsis through shifting the balance of pro-inflammatory and anti-inflammatory c

关键词： Vimentin Sepsis Monocyte Apoptosis Inflammatory cytokine

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Runjing extract promotes spermatogenesis in rats with ornidazole-induced oligoasthenoteratozoospermia through extracellular signal-regulated kinase signalling,and regulating Vimentin expression

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Journal of Traditional Chinese Medicine 2021年第4期41卷 581-587页

作者： YANG Kai LI Shugen ZHANG Tianyu DONG Panpan ZENG Qingqi Department of Andrology Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineZhangjiagang 215600China Department of Urology Suzhou Municipal HospitalSuzhou 215002China Department of Andrology The Affiliated Hospital of Nanjing University of Chinese MedicineNanjing 210029China Department of Andrology Tongde Hospital of Zhejiang ProvinceHangzhou 310012China

OBJECTIVE:To investigate the efficacy of Runjing(RJ)extract on oligoasthenoteratozoospermia(OAT)induced by ornidazole(ORN)in rats,and to study the underlying mechanism.METHODS:Twenty-four adult male Sprague-Dawley rats were treated with normal saline(control),ORN(OAT model),ORN+4.725 g-dose)and ORN+18.9 g·kg^(-1)·d^(-1) RJ extract(low·kg^(-1)·d^(-1) RJ extract(high-dose)for 4 weeks.The rats were then euthanized and sperm and testis samples were collected for analysis.Sperm count,motility and morphology were calculated by sperm suspension from cauda epididymis.Testicular histopathological changes were analyzed by hematoxylin and eosin staining and Td T mediated d UTP nick end labelling.Moreover,the expression of Vimentin and extracellular signal-regulated kinase(ERK)were examined through Western blot,and the distribution of Vimentin was detected via immunohistochemistry.RESULTS:ORN successfully induces seminiferous epithelium injury,cellular apoptosis,and finally OAT(PVimentin and ERK were significantly altered in ORN testes(all PVimentin expression.

关键词： spermatogenesis oligospermia Vimentin extracellular signal-regulated MAP kinases Runjing

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SHP2、E-cadherin、Vimentin在结直肠癌中的表达及临床意义

SHP2、E-cadherin、Vimentin在结直肠癌中的表达及临床意义

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作者：马云涛遵义医科大学

学位级别：硕士

目的:通过研究SHP2、E-cadherin、Vimentin在正常结直肠黏膜、增生性息肉、腺瘤息肉及结直肠癌中的表达及相关性,初步探讨三者在结直肠癌发生发展中的作用和临床意义。方法:收集我院46例结直肠癌及配对癌旁组织、21例结直肠增生息肉及... 详细信息

目的:通过研究SHP2、E-cadherin、Vimentin在正常结直肠黏膜、增生性息肉、腺瘤息肉及结直肠癌中的表达及相关性,初步探讨三者在结直肠癌发生发展中的作用和临床意义。方法:收集我院46例结直肠癌及配对癌旁组织、21例结直肠增生息肉及结直肠腺瘤性息肉组织。采用免疫组织化学法和Western blot技术检测SHP2、E-cadherin、Vimentin蛋白在结直肠正常黏膜、结直肠增生息肉、结直肠腺瘤息肉、结直肠癌组织中的表达水平,分析上述三个指标与结直肠癌患者临床病理特征的关系以及三者之间的相关性。结果:(1)实验结果表明,SHP2在结直肠正常黏膜、结直肠增生性息肉、结直肠腺瘤息肉、结直肠癌组织中的表达强度有逐渐上升的趋势(PVimentin在结直肠正常黏膜存在少量表达,且在结直肠增生性息肉、结直肠腺瘤息肉、结直肠癌组织中的表达水平有逐渐上升的趋势(PVimentin在结直肠癌中的高表达与分化程度差、有淋巴结转移有关。(4)在检测结直肠癌组织中SHP2、E-cadherin、Vimentin蛋白表达后,使用Spearman分析三个指标之间的相关性,结果显示,SHP2与E-cadherin在结直肠癌中的表达呈负相关(r=﹣0.472,PVimentin在结直肠癌中的表达呈正相关(r=0.242,P=0.041);E-cadherin与Vimentin在结直肠癌中的表达呈负相关(r=﹣0.219),但无统计学意义(P=0.064)。结论:(1)SHP2、Vimentin蛋白在结直肠正常黏膜、结直肠增生息肉、结直肠腺瘤性息肉、结直肠癌组织组织中表达逐渐增加。E-cadherin蛋白在上述各组结直肠组织的表达逐渐降低。提示三者在结直肠癌的发生发展中起着一定的作用。(2)SHP2、E-cadherin蛋白的表达与结直肠癌浸润深度、TNM分期、淋巴结转移、脉管侵袭相关;Vimentin蛋白的表达与结直肠癌分化程度、淋巴结转移有关。(3)在结直肠癌中,SHP2与E-cadherin的表达呈负相关;SHP2与Vimentin的表达呈正相关。提示SHP2可能通过调节E-cadherin、Vimentin的表达,促进结直肠癌EMT的发生,从而参与结直肠癌侵袭转移的过程。

关键词：结直肠肿瘤 SHP2 EMT E-cadherin Vimentin

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Expression of Vimentin and glial fibrillary acidic protein in central nervous system development of rats

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Asian Pacific Journal of Tropical Medicine 2017年第12期10卷 1185-1189页

作者： Hua Luo Xiao-Qiong Wu Min Zhao Qiong Wang Geng-Pan Jiang Wei-Jun Cai Ming-Ying Luo Xiangtan Medicine & Health Vocational College XiangtanHunan411104China Department of Anatomy & Neurobiology Xiangya School of MedicineCentral South UniversityChangshaHunan410003China Department of Anatomy & Histology & Embryology Kunming Medical UniversityKunmingYunnan650500China Department of Clinical Medicine Kunming Medical UniversityKunmingYunnan650500China Department of Histology & Embryology Xiangya School of MedicineCentral South UniversityChangshaHunan410003China

Objective: To investigate the distribution and contents of Vimentin(Vim) and glial fibrillary acidic protein(GFAP) immunoreactivities in the central nervous system(CNS)of normal newborn, adult and aged rats.Methods: In this study, thirty healthy and normal Sprague–Dawley rats were simply classified into three groups: Newborn(7 days aged), adult(5 months aged) and aged(24 months aged) rats. Brains and spinal cord were dissected and cut into frozen sections. The expression of Vim and GFAP in CNS were detected by confocal immunofluorescence.Results: In each group, Vim was expressed in all the regions of CNS including the hippocampal, cerebral cortex, the third ventricle and spinal cord, and the expression was highest in neuron-like cell of newborn rats, while Vim was mainly expressed in cell bodies in adult and aged rats. GFAP was expressed in all the regions of CNS including the hippocampal, cerebral cortex, the third ventricle and spinal cord, and the expression was in astrocytes of aged rats. In the third ventricle, Vim was detected in all groups, and only observed in neuron-like cells of newborn. Meanwhile, the GFAP expression showed no significant differences between adult and aged rats in this region. The co-localization of Vim and GFAP were mainly observed in hippocampus and cerebral cortex of newborn,but this co-localization was found in the third ventricle of the rats in all groups.Conclusion: Our data demonstrate for the first time that the expression of Vim and GFAP in the rat's CNS during development. This data may provide a foundation for the further mechanistic studies of these two main intermediate filaments during development of CNS.

关键词： Development Vimentin Glial fibrillary acidic protein Central nervous system

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塞来昔布对大鼠大肠癌E-cadherin、Vimentin、β-catenin表达的影响

塞来昔布对大鼠大肠癌E-cadherin、Vimentin、β-catenin表达的影...

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作者：刘林遵义医科大学

学位级别：硕士

目的:通过塞来昔布干预大鼠大肠肿瘤模型,探讨塞来昔布对大鼠大肠癌组织中EMT相关标记物E-cadherin、Vimentin及β-catenin表达的影响。方法:将30只SD大鼠随机分为5组,即对照组（Control）、模型组（Model）、低剂量塞来昔布干预组（Low... 详细信息

目的:通过塞来昔布干预大鼠大肠肿瘤模型,探讨塞来昔布对大鼠大肠癌组织中EMT相关标记物E-cadherin、Vimentin及β-catenin表达的影响。方法:将30只SD大鼠随机分为5组,即对照组（Control）、模型组（Model）、低剂量塞来昔布干预组（Low dose celecoxib）、中剂量塞来昔布干预组（Medium dose celecoxib）、高剂量塞来昔布干预组（High dose celecoxib）,每组各6只。模型组和各塞来昔布干预组大鼠均腹腔注射二甲基肼,每周一次,共注射20周;同时,各塞来昔布干预组分别予不同浓度塞来昔布溶液灌胃,每天一次,连续给药28周后处死所有大鼠,取大鼠大肠组织进行HE染色明确大鼠大肠肿瘤模型是否构建成功。根据造模结果选取每组大鼠的大肠组织进行实验,采用免疫组化法及Western blot法分别检测E-cadherin、Vimentin及β-catenin蛋白的表达水平,q RT-PCR法检测Vimentin和β-catenin m RNA的相对表达量。结果:1.大鼠大肠肿瘤模型构建结果:除对照组6只大鼠无大肠肿瘤形成外,其余实验大鼠均形成大肠肿瘤。2.免疫组化结果:相比于对照组,模型组E-cadherin蛋白表达下降,Vimentin、β-catenin蛋白表达升高（P＜0.05）;相比于模型组,高剂量塞来昔布干预组E-cadherin蛋白表达升高,Vimentin、β-catenin蛋白表达下降（P＜0.05）。与低剂量塞来昔布干预组相比,高剂量塞来昔布干预组E-cadherin蛋白表达升高,Vimentin、β-catenin蛋白表达下降（P＜0.05）。3.Western blot法结果:相比于对照组,模型组E-cadherin蛋白表达下降,Vimentin、β-catenin蛋白表达升高（P＜0.05）;相比于模型组,中、高剂量塞来昔布干预组E-cadherin蛋白表达升高,Vimentin、β-catenin蛋白表达下降（P＜0.05）;相比于低剂量塞来昔布干预组,高剂量塞来昔布干预组E-cadherin蛋白表达升高,Vimentin、β-catenin蛋白表达下降（P＜0.05）。4.q RT-PCR实验结果:相比于对照组,模型组Vimentin、β-catenin m RNA表达升高（P＜0.05）;相比于模型组,中、高剂量塞来昔布干预组Vimentin、β-catenin m RNA表达下降（P＜0.05）;相比于低剂量塞来昔布干预组,中、高剂量塞来昔布干预组Vimentin、β-catenin m RNA表达下降（P＜0.05）。结论:1.在大鼠大肠癌组织中E-cadherin表达下调,Vimentin及β-catenin表达上调,提示EMT参与了大鼠大肠癌变过程。2.塞来昔布呈剂量依赖性调控大鼠大肠癌中EMT相关标记物的表达,使E-cadherin表达上调,Vimentin及β-catenin表达下调,这表明塞来昔布可在组织水平抑制大肠癌EMT。

关键词：塞来昔布大肠癌 EMT E-cadherin Vimentin β-catenin

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