circPDSS1通过靶向miR-1298调控肝癌细胞侵袭、迁移和凋亡的分子机制

目的 探讨环状RNA PDSS1(circPDSS1)对肝癌细胞凋亡、迁移和侵袭的影响及其机制.方法 实时荧光定量PCR(RT-qPCR)检测肝癌组织、癌旁组织中circPDSS1和miR-1298的表达.双荧光素酶报告基因实验、RT-qPCR确定circPDSS1对miR-1298的靶向调控作用.将circPDSS1...     

circRNA CDR1as靶向miR-876-5p调控肝癌细胞的增殖、迁移和侵袭

目的 研究环状RNA CDR1as对肝癌细胞增殖、迁移和侵袭的影响.方法 运用实时荧光定量-聚合酶链式反应(qRT-PCR)检测正常肝细胞L02和肝癌细胞Huh-7、Hep-3B中CDR1as、miR-876-5p的表达;将si-NC组(转染si-NC)、si-CDR1as组(转染si-CDR1as)、miR-NC组(...     

lncRNA DGCR5通过靶向调控miR-21抑制鼻咽癌细胞的增殖、侵袭和迁移

目的 探讨lncRNA DGCR5对鼻咽癌细胞增殖、迁移和侵袭的影响及其作用机制。方法 将pcDNA-NC、pcDNA-DGCR5、anti-miR-NC、anti-miR-21质粒分别转染至CNE-1、HNE-1细胞中,记为pcDNA-NC组、pcDNA-DGCR5组、anti-miR-NC组、anti-miR-21组;将pcDNA-DGCR5分别与mimic-NC、mimic-miR-21共转染至CNE-1、HNE-1细胞中,记为pcDNA-DGCR5+mimic-NC组、pcDNA-DGCR5+mimic-miR-21组;采用qRT-PCR检测miR-21和DGCR5的表达水平;四甲基偶氮唑蓝(MTT)、Transwell、流式细胞术检测CNE-1、HNE-1细胞增殖活性、迁移、侵袭和凋亡;双荧光素酶报告实验检测DGCR5和miR-21靶向调控。结果 与癌旁组织和人永生化鼻咽上皮细胞NP69相比,鼻咽癌组织和鼻咽癌细胞SUNE-1、CNE-2、CNE-1、HNE-1、HONE-1中DGCR5表达水平显著降低(P<0.05),miR-21表达水平显著增加(P<0.05)...     

miR-409-3p通过调控SLBP影响肝癌细胞的增殖、迁移和侵袭

目的 探讨miR-409-3p对茎环结合蛋白(SLBP)表达的调控作用及其对肝癌细胞增殖、迁移和侵袭的影响.方法 采用qRT-PCR、Western blotting分别检测肝癌组织、癌旁组织及细胞系中miR-409-3p、SLBP的表达水平;以表达量最低的肝癌细胞Hep3B为研究对象,分别将miR-NC、miR-40...     

miR-645靶向EDN3调控肝癌细胞的增殖、迁移和侵袭

目的 探究微小RNA-645(miR-645)是否通过靶向调控内皮素(EDN)3影响肝癌细胞增殖、迁移及侵袭.方法 qRT-PCR法与Western印迹法分别检测miR-645及EDN3 mRNA在不同肝癌细胞及正常肝细胞中的表达;双荧光素酶报告基因系统检测miR-645对EDN3转录活性的影响;噻唑蓝(MTT)实验检...     

lncRNA GAS5通过靶向miR-221抑制骨肉瘤细胞的增殖、迁移和侵袭

目的研究lncRNA生长停滞特异性转录因子(GAS)5在骨肉瘤(OS)细胞U2OS中的表达,并深入探讨GAS5对OS细胞增殖、迁移和侵袭的影响及作用机制。方法 qRT-PCR检测U2OS细胞中GAS5和miR-221的表达;噻唑蓝(MTT)和Transwell小室法分析U2OS细胞的增殖、迁移和侵袭能力;Starbase软件预测GAS5和miR-221的靶向关系,之后采用双荧光素酶报告实验和qRT-PCR分析加以验证。结果与hFOB 1.19组相比,GAS5在U2OS细胞中明显低表达;通过在U2OS细胞中转染pcDNA-GAS5可高效过表达GAS5;外源过表达GAS5可抑制U2OS细胞的增殖、迁移和侵袭能力;GAS5能够与miR-221通过互补位点相互作用;与hFOB 1.19组相比,miR-221在U2OS细胞中明显高表达,且外源过表达miR-221可逆转GAS5对U2OS细胞增殖、迁移和侵袭的抑制作用。结论 GAS5通过降低miR-221表达抑制U2OS细胞的增殖、迁移和侵袭能力,在骨肉瘤中发挥抑癌作用。     

白头翁皂苷A对肝癌细胞增殖、迁移、侵袭和放疗敏感性的影响及机制

目的 探讨白头翁皂苷A(PSA)对肝癌细胞增殖、迁移、侵袭和放疗敏感性的影响及机制.方法 体外培养HepG2细胞,取对数生长期的细胞分别用不同浓度(0、10、15、20 mg/L)PSA进行干预24 h,分别将0、20 mg/L的PSA干预的细胞记为对照组、PSA组.用MTT法检测两组细胞增殖能力,Transwell实...     

金丝桃苷通过抑制HSP90AA1抑制乳腺癌细胞增殖、迁移和侵袭

目的 基于网络药理学方法探讨金丝桃苷治疗乳腺癌的靶点及作用机制,并通过体外和体内实验进行验证。方法 通过SwissTarget和TargetNet数据库获取金丝桃苷作用靶点,通过GeneCards数据库获取乳腺癌疾病相关靶点;利用STRING平台构建蛋白质相互作用(PPI)网络;基于肿瘤基因组图谱(TCGA)数据库分析交集靶点基因与乳腺癌临床表型的关系。采用CCK-8实验及异种移植实验观察金丝桃苷对乳腺癌细胞体外和体内增殖的影响;采用Transwell实验和划痕实验观察金丝桃苷对乳腺癌细胞侵袭和迁移的影响;构建热休克蛋白(HSP)90α家族A类成员(HSP90AA)1过表达质粒并转染人乳腺癌细胞系MCF-7和MDA-MB-231,观察上调HSP90AA1表达对乳腺癌增殖、侵袭及迁移的影响。结果 基于网络药理学的分析显示,金丝桃苷作用于乳腺癌的靶点共有包括HSP90AA1在内的25个靶点;TCGA数据库的临床数据表明,HSP90AA1在乳腺癌癌组织中的表达较正常乳腺组织表达明显上调(P<0.05),且其高表达与临床分期晚及预后差密切相关(P<0.05)。功能实验中,金丝桃苷显...     

抑制Cks1表达对乳腺癌MCF-7细胞增殖、侵袭转移能力的影响及机制探讨

目的观察抑制Cks1表达对人乳腺癌MCF-7细胞增殖、侵袭转移能力的影响,并探讨其机制。方法将MCF-7细胞分为两组,观察组细胞经脂质体转染Cks1siRNA,对照组细胞转染ScrambledsiRNA;分别采用MTS法、Transwell小室实验观察MCF-7细胞的增殖及侵袭转移能力,采用Western blot法检测MCF-7细胞中的MMP-2、MMP-9蛋白。结果观察组转染60、84、108、132h后,MCF-7细胞的OD值分别为0．15±0．01、0．3±0．02、0．7±0．01、1．3±0．02,对照组分别为0．2±0．01、0．5±0．01、1．3±0．03、1．8±0．02,两组转染84、108、132h细胞OD值比较,P均〈0．05。观察组转染48h,侵袭细胞数为（150±17）个、转移细胞数为（210±22）个,对照组分别为（550±90）、（660±96）个,两组比较,P均〈0．05。转染后12h,观察组MMP-2、MMP-9蛋白表达量为0．05±0．002、0．104-0．002,对照组分别为0．95±0．020、0．98±0．030,两组比较,P均〈0．05。结论抑制Cksl表达可显著抑制MCF-7细胞的增殖、侵袭转移能力,该作用可能与MMP-2、MMP-9蛋白表达降低有关。     

COPB2表达对胃癌细胞增殖、迁移和侵袭的影响

背景 外被体蛋白复合物β2亚基(coatomer protein complex subunit beta 2,COPB2)可参与调节多种肿瘤细胞的恶性生物学行为,而其在胃癌中表达和临床意义仍不完全明确.目的 探究COPB2对胃癌细胞增殖、侵袭和迁移能力的影响及其机制.方法 采用免疫组化法观察COPB2在胃癌组织和癌旁...     

microRNA-651-5p affects the proliferation,migration, and invasion of lung cancer cells by regulating Calmodulin 2 expression

Objective

Lung cancer is prevalent worldwide and a leading contributor to tumor death. This research intends to explore the molecular mechanism of the microRNA-651-5p (miR-651-5p)/Calmodulin 2 (CALM2) axis in the proliferation, migration, and invasion of lung cancer cells.

Methods

Lung cancer tissues and para-cancerous tissues were collected. The expression levels of miR-651-5p and CALM2 in lung cancer tissues and cells were tested, and the connection between miR-651-5p expression and clinicopathological characteristics of lung cancer patients was further analyzed. The binding sites between miR-651-5p and CALM2 were analyzed and validated. Lung cancer cell proliferation, migration, invasion, and apoptosis were examined.

Results

miR-651-5p was lowly expressed in lung cancer tissues and cells. miR-651-5p expression had no correlation with patients' age and gender but had a correlation with patients' tumor size, TNM stage, and lymph node metastasis. Overexpression of miR-651-5p repressed proliferative, migratory, and invasive behaviors of lung cancer cells. miR-651-5p targeted and negatively regulated CALM2 expression, and CALM2 reversed the inhibiting effects of miR-651-5p on lung cancer cell malignant behaviors, including proliferation, migration, and invasion.

Conclusion

This study expounds that miR-651-5p affects the proliferation, migration, and invasion of lung cancer cells by regulating CALM2 expression.     

Knockdown of lncRNA TUC338 inhibits esophageal cancer cells migration and invasion

BackgroundLong non-coding RNAs (lncRNAs) are firmly identified with the event and improvement of tumors. Therefore, elucidating the functions and mechanisms of related lncRNAs is significant for understanding the occurrence and advancement of tumors. The recently discovered lncRNA TUC338 has been shown to play the role of an oncogene in an assortment of tumors. Be that as it may, the articulation and elements of lncRNA TUC338 in esophageal cancer are as yet hazy. This investigation plans to explain the capacities and related molecular mechanisms of lncRNA TUC338 in esophageal malignancy.MethodsFirstly, the expression of TUC338 in 50 instances of esophageal disease tissues and nearby tissues was detected by fluorescence reckonable PCR, and correlations with the clinic pathological characteristics of patients was further analyzed. Then, a lentiviral interference vector was designed and transfected into an esophageal cancer cell line, and knockdown was verified by fluorescence quantitative PCR. The effects of TUC338 knockdown on the proliferation, clone formation, and migration and infringement of esophageal malignancy cells were tested utilizing the CCK-8 assay, clone formation experiments, and Transwell experiments. Western blot detected the expression of invasion-related proteins.ResultsFluorescence reckonable PCR exhibit that TUC338 was exceptionally communicated in esophageal cancer tissues, and was significantly related with metastasis and TNM stage in tolerant. Functional experiments showed that in esophageal disease cell lines, knocking down the declaration of TUC338 significantly inhibited cell multiplication, clone development, and intrusion and movement. Further experiments on molecular mechanisms showed that knocking down TUC338 inhibited statement of N-cadherin and vimentin in cells.ConclusionsTUC338 is exceptionally communicated in esophageal malignancy tissues and can regulate cell proliferation and invasion.     

去氢骆驼蓬碱通过下调COX-2表达抑制胃癌细胞迁移和侵袭

目的探讨去氢骆驼蓬碱对人胃癌MKN-45细胞环氧化酶-2(cyclooxygenase-2,COX-2)表达、迁移和侵袭的影响。方法 MKN-45细胞接种于含10%胎牛血清的RPMI-1640培养液中,常规培养24h后加去氢骆驼蓬碱(2、4、8、16、32μg/ml),同时设置对照组不加药物,空白组只加培养液不含细胞,分别培养24h、48h、72h,MTT法检测细胞增殖率;western blot法检测COX-2表达;划痕损伤愈合实验及Transwell小室基质侵袭实验检测胃癌细胞体外迁移和侵袭。结果去氢骆驼蓬碱剂量依赖性抑制MKN-45细胞COX-2表达(P0.01);与对照组相比,去氢骆驼蓬碱组MKN-45细胞迁移和侵袭能力明显下降(P0.01)。结论去氢骆驼蓬碱可能通过下调COX-2表达抑制胃癌细胞迁移和侵袭。     

二甲双胍对肝癌PLC/PRF/5肿瘤干细胞增殖分化、凋亡、迁移的影响

目的:探究二甲双胍对肝癌PLC/PRF/5肿瘤干细胞(CSC)增殖分化、凋亡、迁移的影响。方法:体外特殊条件培养法培养PLC/PRF/5 CSC细胞,用不同浓度(5、10、20 mmol/L)二甲双胍处理PLC/PRF/5 CSC,以未进行处理的PLC/PRF/5 CSC为对照组,在显微镜下观察细胞形态;CCK-8法检测各组细胞活力;流式细胞术检测各组细胞凋亡率;划痕实验检测各组细胞迁移能力;蛋白免疫印迹法检测各组细胞蛋白表达情况;构建裸鼠肝癌移植瘤模型,检测二甲双胍对PLC/PRF/5 CSC成瘤能力的影响。结果:PLC/PRF/5 CSC具有成球能力,经二甲双胍处理后,PLC/PRF/5成球细胞数目显著减少;同一时间段,与对照组比较,二甲双胍处理组细胞活力显著降低,且呈剂量依赖性(P<0.05),随着处理时间的增加,各组细胞活力逐渐降低;与对照组比较,二甲双胍处理组细胞凋亡率、凋亡蛋白Caspase-3、Caspase-9、迁移蛋白E-cadherin的表达显著升高,细胞迁移率、细胞干性基因Oct4、Nanog蛋白表达、迁移蛋白N-cadherin的表达显著降低,且呈剂量依赖性(P<0.05);与对照组比较,随着接种时间的增加,二甲双胍处理组裸鼠肿瘤生长速度较慢(P<0.05),且随着二甲双胍浓度的增加,裸鼠肿瘤生长速度逐渐变慢。结论:二甲双胍能够抑制肝癌PLC/PRF/5 CSC的增殖和迁移,促进其凋亡,可能是靶向肝癌CSC治疗的潜在药物。     

Mir-483 inhibits colon cancer cell proliferation and migration by targeting TRAF1

MicroRNAs are important regulators during human growth and development. Emerging evidence indicates that microRNAs play important roles in colorectal cancer. The aim of this study is to reveal the biological function and direct target gene of miR-483 in colorectal cancer. The biological function of miR-483 on the proliferation and migration of colon cancer cells was then examined by Edu assay and transwell assay, respectively. Our findings revealed that miR-483 mimic could significantly inhibit cell proliferation and migration. The target gene of miR-483 was predicted by target scan software and identified by a dual fluorescence reporter system which showed that TRAF1 was a direct target gene of miR-483 in SW480 cell line. These data suggest that miR-483 is a colorectal cancer suppressor which could inhibit cell proliferation and migration, possibly via targeting TRAF1. The miR-483 could be a potential treatment target for colorectal cancer.     

尼古丁对人A549细胞增殖、侵袭和迁移能力的影响

目的 观察烟草烟雾中的主要有害成分尼古丁对人A549细胞增殖、迁移与侵袭能力的影响,探讨尼古丁致病的可能机制.方法 以一定浓度尼古丁刺激体外培养的人A549细胞,应用CCK-8法、Transwell法和细胞划痕实验分别检测A549细胞的增殖、侵袭及迁移能力.Western blot检测α7烟碱型乙酰胆碱受体(α7 nAChR)、血管内皮生长因子(VEGF)和基质金属蛋白酶2(MMP-2)蛋白的表达.结果 与空白对照组比较,10-6 mol/L尼古丁处理A549细胞后,促进人A549细胞增殖(t=7.920,P<0.05);使穿过基质胶的细胞数增多,侵袭能力增强(t=5.298,P<0.05);使细胞迁移率增加,迁移能力增强(P<0.05).与空白对照组比较,10-6 M尼古丁处理A549细胞24 h后,α7 nAChR、VEGF和MMP-2蛋白表达上调,差异有统计学意义(t值分别为5.800、4.074、6.851,P值均<0.05).结论 尼古丁通过其特异性受体α7 nAChR可增强人A549细胞的增殖、侵袭和迁移能力,其机制可能与VEGF和MMP-2蛋白表达上调有关.