胃癌组织miR-203、miR-4317的表达及临床意义

目的:探讨胃癌组织中微小核糖核酸(mi R)-203、mi R-4317的表达情况及其临床意义。方法:选择2014年1月至2016年12月我院收治的胃癌患者92例,应用实时定量荧光PCR(qRT-PCR)检测患者胃癌组织及其相应癌旁组织中mi R-203、mi R-4317的表达情况,分析mi R-203、mi R-4317表达与胃癌患者临床病理参数的关系,所有患者随访3年,根据mi R-203、mi R-4317在胃癌组织中的中位表达量将患者分为mi R-203高表达组(49例)、mi R-203低表达组(43例)、mi R-4317高表达组(51例)、mi R-4317低表达组(41例)。分析mi R-203、mi R-4317与预后的关系及预后的影响因素。结果:胃癌组织中mi R-203、mi R-4317相对表达量显著低于癌旁组织(P<0.05)。不同性别、年龄、肿瘤大小胃癌患者胃癌组织中mi R-203、mi R-4317相对表达量比较无统计学差异(P>0.05),中低分化、TNM分期为III~IV期、有淋巴结转移胃癌患者胃癌组织中mi R-203、mi R-4317相对表达量显著低于高分化、TNM分期为I~II期、无淋巴结转移胃癌患者(P<0.05)。mi R-203高表达组3年生存率显著高于mi R-203低表达组(P<0.05),mi R-4317高表达组3年生存率显著高于mi R-4317低表达组(P<0.05)。COX多因素分析显示,中低分化、TNM分期为III~IV期、有淋巴结转移、mi R-203低表达、mi R-4317低表达是影响胃癌患者预后的独立危险因素(P<0.05)。结论:胃癌组织中mi R-203、mi R-4317异常低表达,其水平与胃癌预后密切相关,且胃癌患者预后与分化程度、临床分期、淋巴结转移等相关。     

食道癌组织miR-21、miR-182表达与临床病理特征及预后的关系

目的:探讨食道癌组织微小RNA-21(miR-21)、微小RNA-182(miR-182)表达与临床病理特征及预后的关系。方法:选取2011年4月到2013年7月期间在我院接受手术治疗的食道癌患者84例,取患者的癌组织和癌旁正常组织作为检验标本,比较癌组织和癌旁正常组织中miR-21、mi R-182的表达水平,并分析食道癌组织中mi R-182、mi R-21的表达与临床病理特征及预后的关系。结果:癌组织中mi R-21、mi R-182的相对表达量明显高于癌旁正常组织,差异有统计学意义(P<0.05)。食道癌组织中mi R-21的表达与淋巴结转移、临床分期有关(P<0.05),与性别、年龄、分化程度、肿瘤大小无关(P>0.05);食道癌患者癌组织中miR-182的表达与年龄、性别、肿瘤大小无关(P>0.05),与分化程度、临床分期、淋巴结转移有关(P<0.05)。食道癌癌组织中miR-21、miR-182高表达患者的中位生存时间均低于低表达患者,差异有统计学意义(P<0.05)。结论:食道癌组织mi R-21、mi R-182表达与患者的部分临床病理特征及预后有关,两者有望成为食道癌新的治疗靶点。     

非小细胞肺癌患者血清miR-146a、miR-141的表达及临床意义

目的:研究非小细胞肺癌(NSCLC)患者血清微小RNA-146a(mi R-146a)、mi R-141的表达及临床意义。方法:选取2015年1月至2018年1月我院收治的106例NSCLC患者记为NSCLC组,另选取同期于我院进行体检的40例健康体检者记为健康对照组。采用荧光实时定量PCR(qRT-PCR)检测两组血清mi R-146a、mi R-141的表达水平,分析NSCLC患者血清mi R-146a、mi R-141表达水平与临床病理参数的关系,比较血清mi R-146a、mi R-141单一诊断及联合诊断NSCLC的曲线下面积(AUC)、灵敏度、特异度。结果:NSCLC组患者的血清mi R-146a、mi R-141表达水平高于健康对照组(P0.05)。NSCLC患者血清mi R-146a表达水平与病理分期有关(P0.05),与年龄、性别、吸烟史、病理类型、病理分级、肿瘤直径及是否伴有淋巴结转移无关(P0.05)。NSCLC患者血清mi R-141表达水平与病理分期、病理分级及是否伴有淋巴结转移有关(P0.05),与年龄、性别、吸烟史、病理类型、肿瘤直径无关(P0.05)。血清mi R-146a、mi R-141单一诊断及两者联合诊断NSCLC的AUC分别为0.841、0.772、0.921,敏感度分别为85.1%、80.5%、93.5%,特异度分别为84.2%、75.3%、89.8%。结论:NSCLC患者血清mi R-146a、mi R-141表达水平升高,且与部分临床病理参数有关,两者联合检测对NSCLC诊断具有较高的诊断价值。     

靶向miR-592/PIK3CA的lncRNA-XIST对乳腺癌细胞裸鼠的作用机制探究

目的：探讨靶向mi R-592/PIK3CA的lncRNA-XIST对乳腺癌细胞裸鼠的作用机制。方法：选择2021年1月至2022年我院收集的20例乳腺癌组织及癌旁组织,对比lncRNA XIST、mi R-592及PIK3CA的表达水平。培养MCF-10A、MCF-7、BT-549、MDA-MB-468、HSS578T细胞,对比不同乳腺癌细胞中lncRNA XIST、mi R-592及PIK3CA的表达。建立MCF-7裸鼠移植瘤模型建立,将其分为对照组、si-NC组、si-XIST组、pcDNA-NC组、pcDNA-XIST组,对比不同组荷瘤裸鼠生存情况及各组肿瘤体积、抑瘤率。使用Western blot法检测MMP-2、MMP-9、Bax蛋白表达,之后行双荧光素酶报告基因实验。结果：乳腺癌组织中的lncRNA XIST表达水平明显较癌旁组织低,mi R-592、PIK3CA表达水平明显较癌旁组织高（P<0.05）。与MCF-10A正常乳腺癌细胞相比,MCF-7乳腺癌细胞中lncRNA XIST表达最低,mi R-592、PIK3CA表达最高,选择MCF-7乳腺癌细胞作为研究对...     

宫颈癌组织LncRNA HOTAIR、miR-17-5p表达与增殖基因、临床病理特征和预后的关系分析

目的：探讨宫颈癌组织长链非编码核糖核酸（LncRNA）HOX转录反义RNA(HOTAIR)、微小核糖核酸（mi R）-17-5p表达与增殖基因、临床病理特征和预后的关系。方法：选择2014年1月-2018年1月新疆医科大学第一附属医院收治的157例宫颈癌患者,取手术切除的宫颈癌组织和癌旁组织,实时荧光定量聚合酶链反应（RT-PCR）法检测LncRNA HOTAIR、mi R-17-5p及宫颈癌相关增殖基因PRDX4、NEK2、FHIT、BLCAP转录水平表达。Pearson分析宫颈癌组织LncRNA HOTAIR、mi R-17-5p表达与增殖基因表达的相关性,Kaplan-Meier法分析不同LncRNA HOTAIR、mi R-17-5p表达宫颈癌患者的5年生存率差异。结果：宫颈癌组织LncRNA HOTAIR、mi R-17-5p、PRDX4、NEK2、FHIT、BLCAP转录水平表达均高于癌旁组织（P<0.05）。宫颈癌组织LncRNA HOTAIR、mi R-17-5p表达与PRDX4、NEK2、FHIT、BLCAP转录水平表达均呈正相关（P<0.05）,LncR...     

miR-199a-3p负调控CBX7影响肺癌细胞NCI-H460的生物学行为研究

目的:探讨mi R-199a-3p负调控CBX7影响肺癌细胞NCI-H460的生物学行为。方法:qRT-PCR法检测并比较肺癌组织、癌旁正常组织、肺癌细胞、正常肺上皮细胞中的mi R-199a-3p m RNA相对表达量。比较远处转移肺癌组织、未转移肺癌组织中mi R-199a-3p m RNA相对表达量。qRT-PCR法、Western Blot法检测并比较肺癌组织、癌旁正常组织中的CBX7 m RNA及蛋白的表达水平。荧光素酶活性法检测mi R-199a-3p与靶基因CBX7的结合。比较mi R-199a-3p模拟物转染组与阴性对照组的肺癌细胞中的CBX7 m RNA相对表达量及CBX7蛋白表达水平。CCK8实验检测mi R-199a-3p对肺癌细胞增殖的促进作用。Tranwell实验检测mi R-199a-3p对肺癌细胞侵袭与迁移能力的影响。结果:肺癌组织中mi R-199a-3p明显高于癌旁正常组织,发生远处转移的肺癌组织中mi R-199a-3p m RNA的表达量明显高于未发生转移的肺癌组织,差异有统计学意义(P<0.001)。肺癌组织中CBX7m RNA、CBX7蛋白表达水平均明显低于癌旁正常组织,差异有统计学意义(P<0.001)。荧光素酶活性法证实mi R-199a-3p可与靶基因CBX7结合抑制CBX7的表达。肺癌细胞中mi R-199a-3p m RNA的相对表达量明显高于正常肺上皮细胞,CBX7 m RNA相对表达量明显低于正常肺上皮细胞(P<0.05)。对于肺癌细胞,mi R-199a-3p模拟物转染组的CBX7 m RNA相对表达量及CBX7蛋白表达水平均明显低于阴性对照组(P<0.001)。CCK8实验证实mi R-199a-3p能够促进肺癌细胞的增殖,Tranwell实验证实mi R-199a-3p对肺癌细胞侵袭与迁移具有积极的促进作用。结论:mi R-199a-3p在肺癌的发生发展过程中发挥重要作用,能够通过抑制CBX7基因的表达,促进肺癌细胞的增殖、侵袭和转移。     

miR-106b-93-25簇对子宫内膜癌细胞的调控作用研究

目的:检测mi R-106b-93-25基因簇对子宫内膜癌细胞增殖及凋亡的影响,并探讨其机制。方法:q RT-PCR检测临床子宫内膜癌标本及癌旁正常组织中mi R-106b、mi R-93和mi R-25及其宿主基因MCM7的表达情况。将micro RNA及其拮抗剂转染ECC-1细胞后,MTT实验检测ECC-1细胞增殖情况,流式细胞术检测ECC-1细胞周期及细胞凋亡情况。荧光素酶报告系统验证mi R-106b和mi R-25分别直接调控p21和Bim。结果:临床标本子宫内膜癌组织与癌旁正常组织相比mi R-106b-93-25簇及其宿主基因MCM7的表达明显增高。mi R-106b-93-25簇能够促进ECC-1细胞增殖,减少凋亡。转染mi R-106b和mi R-93的细胞出现明显的S期阻滞,过表达mi R-25的细胞凋亡明显减少。mi R-106b-93-25簇通过抑制靶基因p21和Bim的表达,引起促增殖、抗凋亡作用。结论:mi R-106b-93-25簇能够促进子宫内膜癌细胞增殖,抑制凋亡,并使细胞发生S期阻滞。mi R-106b-93-25簇在子宫内膜癌的发生与发展中具有重要的作用。     

miR-125b靶向MCL1抑制胃癌 MGC-803细胞增殖

探讨mi R-125b对胃癌MGC-803细胞增殖的影响及机制,为阐明胃癌发病的分子机制提供实验依据.采用q RT-PCR和原位杂交,检测mi R-125b在正常胃黏膜(NGM)和胃癌(GAC)组织中的表达.将mi R-125b导入胃癌MGC-803细胞,观察mi R-125b高表达对MGC-803细胞增殖的影响.利用Targetscan 6.2软件及荧光素酶报告基因检测,分析mi R-125b对MCL1基因的靶向性作用.构建MCL1干扰载体,观察干扰MCL1基因表达对MGC-803细胞增殖的影响.结果发现,mi R-125b在胃癌组织中低表达,其表达与胃癌的分化程度及患者预后呈正相关,与TNM分期、淋巴结转移呈负相关(P0.01).mi R-125b高表达后MGC-803细胞的增殖降低、凋亡率增加、裂解caspase-3与裂解PARP表达增加(P0.01);mi R-125b与MCL1基因的3′UTR(2 613~2 620)结合,抑制MCL1的m RNA及蛋白质表达(P0.01);沉默MCL1基因表达后MGC-803细胞的增殖降低、凋亡率增加、裂解caspase-3与裂解PARP表达增加(P0.01).从而得出结论,mi R-125b在胃癌组织中低表达,其表达与胃癌组织分化程度、TNM分期、淋巴结转移及患者预后密切相关;mi R-125b靶向抑制MCL1基因表达,活化caspase-3信号通路,抑制MGC-803细胞增殖.     

miR-448通过抑制上皮间质转化抑制肺癌细胞增殖和运动能力

探讨mi R-448对肺癌细胞增殖和运动的影响及其分子机制。采用实时荧光定量PCR(polymerase chain reaction)检测原发肺癌组织和癌旁正常组织mi R-448表达水平。转染mi R-448 mimic和inhibitor至肺癌A549细胞系,通过MTT(3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide)、平板克隆形成和Transwell实验观察mi R-448表达对A549增殖和运动能力的影响;利用Western blot检测EMT(epithelial-mesenchymal transition)标志物蛋白表达水平,通过实时荧光定量PCR检测EMT相关转录因子m RNA表达水平。实时荧光定量PCR显示较癌旁正常组织相比,mi R-448在原发肺癌组织中表达降低。MTT和平板克隆形成实验显示,过表达mi R-448抑制A549细胞增殖和运动能力;降表达mi R-448增强A549细胞增殖和运动能力。Western blot显示降表达mi R-448能下调上皮标志物E-cadherin,上调间质标志物Vimentin表达水平。实时荧光定量PCR显示降表达mi R-448能上调EMT相关转录因子Twist1和ZEB1 m RNA表达水平。mi R-448可通过抑制EMT抑制肺癌进展。     

miR-17-92、自噬在肿瘤中的研究进展

micro RNA(mi RNA)是一类在转录后水平调控目的基因表达的功能性小RNA分子。mi R-17-92基因簇是一个高度保守的基因簇,编码6个mi RNAs,分别为:mi R-17、mi R-18a、mi R-19a、mi R-19b-1、mi R-20a和mi R-92a。细胞自噬(autophagy)是将细胞内受损、变性或衰老的蛋白质以及细胞器运输到溶酶体进行消化降解的过程。mi RNA的异常表达可影响自噬水平,从而影响肿瘤的发生发展。研究证明mi R-17-92基因簇与细胞自噬及肿瘤的发生密切相关,有望成为具有潜在价值的肿瘤标志物或肿瘤治疗的新靶点。现对mi R-17-92基因簇与细胞自噬和肿瘤的关系进行综述。     

MARVELD1调控内含子miR-186、miR-335表达的研究

目的:前期研究发现,MARVELD1(具有囊泡运输和膜连接功能的MAL及相关蛋白1)在多种肿瘤细胞中表达下调,许多micro RNAs也随其发生变化。本研究探讨了MARVELD1调控mi R-186和mi R-335的表达方式。方法:本研究选取了多种肺癌细胞系,运用q RT-PCR的方法检测了MARVELD1以及mi R-186和mi R-335的表达情况,通过MARVELD1过表达体系和si RNA干扰MARVELD1表达的体系分析mi R-186和mi R-335表达变化情况,运用生物信息学网站对mi R-186和mi R-335进行分析,确认其是否为内含子mi RNA,并进一步应用MARVELD1过表达和RNAi体系检测MARVELD1对mi R-186和mi R-335的宿主基因的影响。结果:在肺癌细胞中,MARVELD1与mi R-186、mi R-335的表达呈现明显的正相关。在过表达MARVELD1之后,mi R-186、mi R-335出现高表达;当下调MARVELD1表达时,mi R-186、mi R-335则表现低表达。生物信息学分析发现mi R-186和mi R-335均为内含子mi RNA。进一步分析MARVELD1与mi R-186和mi R-335宿主基因的表达关系显示,MARVELD1可以上调它们的宿主基因的表达。结论:上述结果表明,MARVELD1可通过影响内含子mi R-186和mi R-335的宿主基因进而调控二者的表达,为进一步研究MARVELD1影响肿瘤细胞的发生机制奠定了基础。     

Circulating miR-3613-5p but not miR-125b-5p,miR-199a-3p,and miR-451a are biomarkers of endometriosis

ObjectiveThis study aimed to assess the utility of circulating miR-125b-5p, miR-199a-3p, miR-451a, and miR-3613-5p as biomarkers of endometriosis.Study designPatients with stage III or IV of endometriosis according to the revised American Society of Reproductive Medicine (rASRM) staging classification, as well as control women, were recruited. We created a prospective study conducted on a group of 48 patients (n = 25 controls, n = 24 endometriosis) who had laparoscopic surgery. Blood samples were taken and plasma miRNA levels were measured by quantitative real-time polymerase chain reaction (RT-qPCR) and assessed with AUC and ROC curves.ResultsMiR-451a and miR-3613-5p were significantly decreased in the plasma of endometriosis patients. miR-451a had a receiver-operating characteristic (ROC) area under the curve 0.8283 and miR-3613-5p had a ROC area under the curve 0.7617. The concentration of circulating miR-125b-5p and miR-199-3p did not differ between endometriosis patients and controls. Plasma miRNA levels did not change with BMI, smoking status, fertility problems, or menstrual pain according to the VAS scale (p > 0.05).ConclusionCirculating miR-451a and miR-3613-5p levels significantly differed between endometriosis and controls. However, the levels of miR-451a were discordant with previous studies. Therefore, miR-3613-5p may have better potential as the endometriosis biomarker. Circulating miR-125b-5p and miR-199a-3p cannot be used as reliable markers of endometriosis.     

脑胶质瘤组织miR-211、miR-374、miR-510表达水平与临床病理特征及预后的关系研究

摘要 目的：探讨脑胶质瘤组织微小RNA（miR）-211、miR-374、miR-510表达水平与临床病理特征及预后的关系。方法：选择2013年8月至2015年8月我院诊治的83例脑胶质瘤患者作为研究对象,选择同期由于脑外伤在我院行内减压术切除的正常脑组织样本31份作为对照样本。采用荧光定量PCR检测miR-211、miR-374、miR-510表达水平,生存分析采用Kaplan-Meier法,应用Cox比例风险回归模型分析预后的影响因素。结果：与正常脑组织相比,脑胶质瘤组织中miR-211、miR-374表达水平明显下降,miR-510表达水平明显升高（P<0.05）。脑胶质瘤组织miR-211、miR-374、miR-510表达均与WHO分级和卡氏功能状态量表(KPS)评分有关（P<0.05）。miR-211、miR-374低表达患者的5年总生存率明显低于高表达患者,miR-510低表达患者的5年总生存率明显高于高表达患者（P<0.05）。WHO分级、KPS评分、miR-211、miR-374和miR-510表达是脑胶质瘤患者预后的影响因素（P<0.05）。结论：脑胶质瘤组织中miR-211和miR-374表达下调,而miR-510表达上调,miR-211、miR-374和miR-510表达均与WHO分级、KPS评分和预后相关,检测miR-211、miR-374和miR-51在脑胶质瘤患者的诊断和治疗中具有一定临床意义。     

miR-30a和miR-30b靶向GW182的生物学功能研究

目的：通过证明miR-30a、miR-30b靶向GW182,探索HeLa细胞中miR-30a、miR-30b及GW182的生物学功能。方法：生物信息学预测分析表明GW182的3＇UTR区存在4个保守的miR-30a、miR-30b靶位点,将含有靶位点的序列片段构建到萤光素酶报告载体中,检测miR-30a、miR-30b与靶位点的结合情况;用阳离子脂质体转染GW182 siRNA和miR-30a、miR-30b mimics,检测GW182下游功能的变化。结果：miR-30a、miR-30b能够靶向GW182;qPCR及Western印迹证明miR-30a、miR-30b可以在mRNA与蛋白水平上降低GW182的表达,同时影响GW182所参与的miRNA/siRNA对靶基因的抑制作用。结论：GW182是miR-30a、miR-30b的靶基因,揭示了miR-30a、miR-30b通过靶向GW182影响miRNA/siRNA作用途径的新功能。     

LINC00467 promotes cell proliferation and stemness in lung adenocarcinoma by sponging miR-4779 and miR-7978

Lung adenocarcinoma (LAD), as one of the most common types of lung tumors, is lethal and malignant. Long noncoding RNAs (lncRNAs) play important roles in various cancers according to many previous studies. LINC00467 was proposed to be a tumor promoter. Despite the validated promotive effect of LINC00467 on neuroblastoma progression, its regulatory mechanism in LAD remains unclear. In this study, LINC00467 expressed higher in LAD tissues and cell lines, and increased LINC00467 indicated a poor prognosis. Knockdown of LINC00467 inhibited cell proliferation, the expressions of tumor stem cell-related genes, and cell spheroid formation ability, while it promoted cell apoptosis. miR-4779 and miR-7978 were reported to play antitumor roles in several cancers before. LINC00467 could combine with miR-4779 and miR-7978, and negatively regulated miR-4779 and miR-7978. miR-4779 and miR-7978 inhibitor could partly rescue the LINC00467 knockdown-induced influence on cell proliferation, apoptosis, and stemness. In a word, this study innovatively investigated the mechanism of LINC00467 in LAD and verified LINC00467 exerted its carcinogenesis function by sponging miR-4779 and miR-7978, which may become a catalyst for generating new therapeutic targets for LAD treatment.     

Dysregulation of exosomal miR-192 and miR-194 expression in lung adenocarcinoma patients

Non-small cell lung cancer (NSCLC) is the main reason of cancer linked mortality and around 80% of cases diagnosed in advanced stage. Therefore current study designed to evaluate the deregulation of miRNA-194 and miRNA-192 in different body fluid of Non small cell lung cancer participants. Present study recruited newly diagnosed histopathologically confirmed. It was observed that the 40% NSCLC participants showed elevated miR-194 expression and 60% NSCLC participants showed reduced miR-194 expression in serum sample while in Bronchial wash, only 20% NSCLC participants showed elevated miR-194 expression while 80% showed reduced miR-194 expression (p = 0.003). It was found that the 54% NSCLC participants showed elevated miR-192 expression and 55% NSCLC participants showed reduced miR-192 expression in serum sample while In Bronchial wash sample, only 25% NSCLC participants showed high miR-192 expression while 75% showed low miR-192 expression (P = 0.0004). Expression of miR-194 was significantly associated with TNM stages (p < 0.0001, p < 0.0001), distant organ metastases (p < 0.0001, p < 0.0001), pathological grade (p = 0.0009, p = 0.0005) among serum sample and bronchial wash sample. Same observation was found with expression of miR-192 and it was significantly associated with TNM stages (p < 0.0001, p < 0.0001), distant organ metastases (p < 0.0001, p < 0.0001), pathological grade (p = 0.006, p = 0.001) among serum sample and bronchial wash sample. It was observed that the NSCLC participants who had high serum based miR-194 expression showed 22 months of overall median survival while low expression of serum based miR-194 expression showed 18 months of overall median survival. Present study suggests that decreased expression of miR-194 and miR-192 was significantly associated with different clinical features of NSCLC cases. However, significantly higher number of NSCLC cases showed low expression of miR-194 and miR-192 in bronchial lavage sample. Decreased poor overall survival was found to be associated with bronchial wash sample with respect to low miR-194 and miR-192 expression while NSCLC participants showed better overall survival with high miR-194 and miR-192 expression. This suggested decreased expression of miR-192 and miR-194 expression could be the potential prognostic marker among NSCLC participants.     

骨髓基质干细胞诱导分化为神经元过程中miR-124和miR-128的表达

目的探讨骨髓基质干细胞诱导分化为神经元过程中miR-124和miR-128的表达变化及作用。方法采用全骨髓培养法体外分离培养获得骨髓基质干细胞,取传代培养至第3代的骨髓基质干细胞,在神经干细胞培养液及细胞因子等条件下诱导其分化为神经元,倒置显微镜下观察其形态变化,应用ABI公司的TaqManMicroRNAAssaysreal-timePCR技术,检测miR-124和miR-128在诱导分化过程中的表达。结果 miR-124分化后神经元的表达是未分化BMSCs的0.051倍(P0.05);miR-128分化后神经元的表达是未分化BMSCs的0.070倍(P0.05)。结论 miR-124和miR-128在骨髓基质干细胞诱导分化为神经元过程中可能起重要作用。     

miR-15a 和miR-16-1 模拟物对人骨肉瘤细胞系SOSP-9607 凋亡 和增殖的影响

目的:探讨miR-15a和miR-16-1模拟物对于人骨肉瘤细胞系SOSP-9607凋亡和增殖的影响。方法:将SOSP-9607细胞分为实验组和对照组。实验组分为miR-15a组、miR-16-1组、miR-15a+miR-16-1组。以miR-15a组为例,采用miR-15a模拟物(hsa-miR-15a mimics)上调SOSP-9607细胞内的miR-15a表达量。对照组分为阴性对照组和空白对照组。采用流式细胞仪测定细胞凋亡率,四甲基偶氮唑蓝(MTT)法测定细胞增殖,并计算细胞增殖效率。结果:通过统计学分析,实验组凋亡率与阴性对照组凋亡率相比明显增高(P<0.05);实验组的细胞增殖率明显低于对照组(P<0.05)。结论:上调SOSP-9607细胞内miR-15a和miR-16-1的表达量可促进SOSP-9607细胞的凋亡并抑制其增殖。     

Suppressive effect of exogenous miR-16 and miR-34a on tumorigenesis of breast cancer cells

Recent investigations have shown tumor-suppressive roles for miR-16 and miR-34a. They also share some features in regard to targeting cancer cell signaling pathways which they control. Therefore, in this study, we aimed to further scrutinize whether exogenous induction of mature miR-34a and miR-16 can collaborate in breast tumor suppression. MDA-MB-231 and SK-BR-3 human breast cancer cell lines were cultured and transfected twice with hsa-miR-16-5p and hsa-miR-34a-5p mimics individually or in combination. The cells were analyzed for apoptosis rate and cell cycle indices by flow cytometry. Also, the expression of several invasion and the epithelial-mesenchymal transition markers was evaluated at gene and protein levels by quantitative real-time polymerase chain reaction and western blot analysis, respectively. Assessment of invasiveness and migratory potential of the transfected cells was performed using three-dimensional spheroid formation and wound-healing assay, respectively. In both cell lines, miR-16 and miR-34a induced apoptosis and cell-cycle arrest and also suppressed invasion and migration. Some of these effects, like cell-cycle arrest and induction of apoptosis, were significantly higher when using both microRNAs than when using them individually for transfection of the cells. Our results are indicating that miR-16 and miR-34a can collaborate in breast tumor suppression.