miR-148b在肺腺癌中的表达及其功能分析

目的 探讨微小RNA-148b（miR-148b）在肺腺癌组织和细胞株中的表达及临床意义。方法 采用实时定量PCR检测13例肺腺癌及癌旁组织中miR-148b的表达,并检测其在肺腺癌细胞株H1437、H1975、A549、PC14/B和正常人肺上皮细胞株HBE中的表达,选取肺腺癌细胞株miR-148b表达水平最低者分别转染miR-148b模拟物（mimics）和miR-148b control。通过MTT检测、低密度细胞集落形成实验、Transwell实验检测miR-148b对细胞增殖、集落形成和侵袭能力的影响。结果 miR-148b在肺腺癌和癌旁组织中的相对表达量分别为0.61±0.42和0.91±0.32（P＜0.05）;与正常肺上皮细胞株HBE（相对表达量设为1.00）比较,4种肺腺癌细胞株H1437、H1975、A549、PC14/B中miR-148b的表达量分别为0.42±0.08、0.38±0.02、0.29±0.03和0.21±0.04（P＜0.05）,选取PC14/B细胞株进行后续实验。MTT检测显示,实验第3天,转染miR-148b mimics的PC14/B细胞吸光值明显低于转染miR-148b control组（P＜0.05）;低密度细胞集落形成实验中,与转染了miR-148b control的PC14/B细胞（相对克隆数设为100）相比,转染miR-148b mimics的PC14/B细胞的相对克隆数为47±8,差异有统计学意义（P＜0.05）;Transwell实验显示,转染miR-148b mimics后穿过基底膜的相对PC14/B细胞数为82±22,与miR-148b control组（200±34）相比,差异有统计学意义（P＜0.05）。结论 miR-148b在肺腺癌组织和细胞中表达下调,且可抑制肺腺癌PC14/B细胞株的增殖、集落形成和侵袭能力。     

Down-regulation of miR-106b suppresses the growth of human glioma cells

Recently, many studies have found that the miR-106b ~25 cluster plays an oncogenic role in tumor progression. However, the precise role of each microRNAs (miRNAs) in the cluster is not yet clear. In the present study, we examined the expression of miR-106b in glioma samples and a tissue microarray by real-time PCR and in situ hybridization (ISH), respectively, finding that miR-106b is overexpressed in the majority of gliomas. Meanwhile, the expression of miR-106b was positively correlated with tumor grade (p < 0.05). The transfection of a miR-106b anti-sense oligonucleotide (ASON) into three human glioma cell lines (U251, LN229 and TJ905) suppressed the proliferation of these cells. Moreover, the growth of xenograft tumors in nude mice treated with miR-106b ASON was significantly impaired. A bioinformatics analysis predicted that RBL2 may be the target of miR-106b, and dual-luciferase reporter assays identified RBL2, but not RB1 or RBL1, as a target of miR-106b. These results suggest that miR-106b facilitates glioma cell growth by promoting cell cycle progression through the negative regulation of RBL2.     

Expression level of human miR-34a correlates with glioma grade and prognosis

The aim of this study is to investigate the expression level of microRNA-34a (miR-34a) in glioma patients and its significance for predicting the prognosis of glioma. In this study, we examined the expression of miR-34a in glioma tissues of various World Health Organization (WHO) grades and explored the association between miR-34a expression and clinical and pathological parameters of glioma patients. We found that the tissues from high-grade gliomas (grade III and IV) had much lower miR-34a expression compared to normal brain tissues. The results of a 72-month follow-up in 146 glioma patients further demonstrated that miR-34a expression levels positively correlated with tumor WHO grades. Additionally, in the patients with grade III and IV gliomas, lower miR-34a expression correlated with worse progression-free survival and overall survival. Univariate and multivariate analysis revealed that miR-34a was an independent prognostic indicator for glioma. Additionally, we explored the correlation between miR-34a expression and p53 status and Bcl-2 expression in grade III and IV glioma tissues. Wild-type p53 tumors displayed significantly higher miR-34a expression level than mutant p53 tumors. In addition, glioma tissues with high miR-34a expression had dramatically lower Bcl-2 expression levels than tissues with low miR-34a expression. These findings indicate the role of miR-34a in tumor progression may be closely associated with p53 mutation and inversely correlated to Bcl-2 expression. In conclusion, our work presents comprehensive evidence for miR-34a expression as a novel and potentially useful signature for predicting prognosis of glioma.     

miR-34b表达调控及其在肿瘤发生中作用的研究进展

miRNA是一种内源性的非编码小RNA,在转录后水平调控基因表达,具有高度保守性和组织特异性.其广泛参与调控细胞的生长、发育等许多复杂生命过程,在多种肿瘤的发病中起重要作用.miR-34b为新近发现并备受关注的miRNA之一,受p53及其启动子甲基化等因素的调节,并通过调控多种靶分子参与调节细胞的增殖与凋亡,对肿瘤的发生与调控起作用,在肿瘤的治疗与预后中有广阔的应用前景.文章就miR-34b及其与肿瘤关系的研究进展进行综述.     

Role of miR-27a,miR-181a and miR-20b in gastric cancer hypoxia-induced chemoresistance

Despite the search for new therapeutic strategies for gastric cancer (GC), there is much evidence of progression due to resistance to chemotherapy. Multidrug resistance (MDR) is the ability of cancer cells to survive after exposure to chemotherapeutic agents. The involvement of miRNAs in the development of MDR has been well described but miRNAs able to modulate the sensitivity to chemotherapy by regulating hypoxia signaling pathways have not yet been fully addressed in GC. Our aim was to analyze miR-20b, miR-27a and miR-181a expression with respect to (epirubicin/oxaliplatin/capecitabine (EOX)) chemotherapy regimen in a set of GC patients, in order to investigate whether miRNAs deregulation may influence GC MDR also via hypoxia signaling modulation. Cancer biopsy were obtained from 21 untreated HER2 negative advanced GC patients, retrospectively analyzed. All patients received a first-line chemotherapy (EOX) regimen. MirWalk database was used to identify miR-27a, miR-181a and miR-20b target genes. The expression of miRNAs and of HIPK2, HIF1A and MDR1 genes were detected by real-time PCR. HIPK2 localization was assessed by immunohistochemistry. Our data showed the down-regulation of miR-20b, miR-27a, miR-181a concomitantly to higher levels of MDR1, HIF1A and HIPK2 genes in GC patients with a progressive disease respect to those with a disease control rate. Moreover, immunohistochemistry assay highlighted a higher cytoplasmic HIPK2 staining, suggesting a different role for it. We showed that aberrant expression of miR-20b, miR27a and miR-181a was associated with chemotherapeutic response in GC through HIF1A, MDR1 and HIPK2 genes modulation, suggesting a possible novel therapeutic strategy.     

A predicted miR-27a-mediated network identifies a signature of glioma

The dysregulation of physiological microRNA (miRNA) activity has been shown to play an important role in gliomagenesis. In a previous study, using microRNA arrays and glioma tissues found that miR-27a was upregulated, which was also identified in the glioma cell lines and samples by quantitative real-time polymerase chain reaction (qRT-PCR). In this study, in order to explore the potential roles of miR-27a in the progression of glioma, we first utilized text-mining of PubMed abstracts with natural language processing (NLP) to identify 1,168 glioma-related molecules. In addition, miR-27a targets predicted by computational methods were integrated with the results from NLP analysis, followed by Gene Ontology (GO), pathway and network analysis. We identified 33?hub genes by overlap calculation and demonstrated that miR-27a may be involved in the progression of glioma through adherens junction, focal adhesion, the neurotrophin signaling pathway, the MAPK signaling pathway, the transforming growth factor-β (TGF-β) signaling pathway, cytokine-cytokine receptor interactions, the p53 signaling pathway, the apoptotic signaling pathway, as well as others. Our data may provide researchers with a better understanding of the mechanisms of the miR-27a-target network in glioma initiation and progression.     

miR-125b抑制胶质瘤细胞增殖作用机制研究

目的 探讨 miR-125b抑制胶质瘤细胞增殖的分子作用机制。方法 选取2016年12月至2017年12月宁夏医科大学总医院收治的胶质瘤患者32例（男18例、女14例）,选择同期行脑内血肿清除术的脑出血或因颅脑损伤行颅内减压术的但脑组织正常患者31例为对照组（男15 例、女 16 例）。利用qPCR法检测miR-125b在胶质瘤组织和人胶质瘤细胞系 LN229的表达,通过转染miR-125b 模拟物,检测miR-125b对胶质瘤细胞LN229增殖的抑制作用,采用Targetscan、miRanda等预测软件对miR-125b的作用靶点进行预测,以双荧光素酶报告基因系统分析miR-125b与STAT3的相互作用,运用Western blot法检测miR-125b对胶质瘤细胞LN229中STAT3表达的影响。结果 与正常癌旁脑组织相比较,胶质瘤组织中miR-125b的表达水平明显降低,胶质瘤细胞系LN229中miR-125b的表达与正常星形胶质细胞明显降低,相比于NC 模拟物,转染miR-125b 模拟物之后LN229细胞的增殖显著抑制,双荧光素酶报告基因系统检测显示,miR-125b 可直接调控STAT3 转录活性,而且miR-125b显著抑制LN229细胞STAT3表达。结论 miR-125b可靶向STAT3的表达从而调控胶质瘤细胞的增殖。     

miR-34b和miR-155在膀胱尿路上皮癌中的表达及意义

目的:检测miR-34b和miR-155在膀胱尿路上皮癌中的表达,分析其在不同临床病理特征中的表达差别。方法:选取2014年1月至2016年1月我院收治的79例膀胱尿路上皮癌患者为观察组,选取距肿物边缘>3 cm的正常膀胱黏膜组织52例作为对照组,应用实时荧光定量PCR法检测两组中miR-34b和miR-155的表达情况。结果:两组中miR-34b和miR-155的表达差别有统计学意义,观察组中miR-34b和miR-155的表达在不同病变级别、是否浸润、脉管癌栓、淋巴结转移及TNM分期的表达中差别有统计学意义。观察组中miR-34b的表达与增殖指数间呈负相关性,miR-155的表达与增殖指数间呈正相关性。生存分析显示二者的表达与生存时间有关。结论:膀胱尿路上皮癌组织中miR-34b低表达、miR-155高表达,对病变的形成和进展有重要的促进作用。二者对肿瘤的作用可能与对细胞增殖的促进作用有关。术后检测miR-34b和miR-155的表达对判断预后可能有一定价值。     

Expression of miR-125b in the new, highly invasive glioma stem cell and progenitor cell line SU3

MicroRNA (miR)-125b has been shown to play a potential role in the development of glioma stem cells.However,the relationship between miRNA and glioma stem cells is still elusive.This study was designed to elucidate this potential relationship.We established a highly invasive glioma stem cell and progenitor (GSCP) cell line SU3.SU3 cell suspensions were injected into nude mice brains in situ,and the invasiveness of graft tumors was analyzed using hematoxylin and eosin staining as well as immunohistochemistry.Real-time polymerase chain reaction (PCR) was used to measure the expression levels of miR-125b in SU3 and other cells.In vitro,SU3 cells expressed CD133 and nestin as well as differentiation markers glial fibrillary acidic protein (GFAP) and β-tubulin III,which were consistent with the characteristics of glioma stem cells.Scratch assays indicated that the migration ability of SU3 cells was stronger than that of U251 stem cells (U251s).In vivo,SU3 cells invaded into each part of the mouse brain from the caudate nucleus in a diffuse pattern and highly expressed invasive and proliferative cell markers matrix metalloprotease 2 (MMP2),MMP9,and Ki-67.Real-time PCR results revealed that the levels of miR-125b and MMP9 were significantly higher in SU3 and SU2,also a highly invasive GSCP cell line we established before,than in U251s.High expression of miR-125b both in newly established GSCPs,SU3,and long-term cultured GSCPs,SU2 suggests that miR-125b exhibits oncogene-like behavior.This behavior should be considered in further studies of miR-125b in cancer stem cells.Furthermore,MMP9,which plays a role in cancer stem cell invasion,may be a target gene of miR-125b.     

胶质瘤细胞诱导分化相关基因在胶质瘤组织中的表达

目的 利用已经建立的胶质瘤细胞诱导分化相关基因表达谱，筛选胶质瘤恶性进展相关基因。方法 按分子生物学实验要求，收集经病理确诊的不同恶性程度胶质瘤手术标本，应用反向多点杂交技术制作分子探针，与96个相关基因组成的小芯片杂交检测在不同恶性级别胶质瘤手术标本中的表达情况。结果共有8个基因在各个恶性级别胶质瘤中均呈高表达；有14个基因随胶质瘤恶性程度升高而表达频率呈上升趋势；有6个基因随胶质瘤恶性程度升高表达频率呈下降趋势；筛选到可能与胶质瘤恶性进展有关的新基因有DIP1、RPS7、CLK2、WWOX／FOR、GRIM-19等基因。结论 本研究制作的胶质瘤细胞分化相关基因小芯片，在不同级别胶质瘤组织标本中检测到的表达情况，可进一步用于胶质瘤恶性进展的分子机制研究。     

miR-19a和miR-19b在骨肉瘤中的表达及其临床意义

目的：探讨miR-19a和miR-19b在骨肉瘤组织及配对瘤旁组织中的表达及其与临床病理特征的相关性。方法：收集32对骨肉瘤和配对的瘤旁组织,运用实时荧光定量PCR（qPCR）检测骨肉瘤组织及其瘤旁组织中miR-19a和miR-19b的表达,分析其与骨肉瘤临床病理特征的相关性及其临床意义。结果：qPCR结果显示骨肉瘤组织中miR-19a和miR-19b的平均表达量较瘤旁组织中均明显上调（P均 < 0.05）。二者的表达水平呈正相关（r=0.685,P=0.000）。miR-19a和miR-19b的表达与骨肉瘤病理分级之间存在正相关（r=0.478,P=0.027）;miR-19a的表达与临床分期呈正相关（r=0.365,P=0.031）且与预后相关。Cox回归多因素分析发现miR-19a可作为骨肉瘤患者预后的影响因子（P=0.037）。结论：miR-19a和miR-19b在骨肉瘤中表达上调,在骨肉瘤的发生发展中可能发挥重要的作用,其中miR-19a可能作为骨肉瘤独立的预后标志物。     

微小RNA-133b在胃癌中的表达及意义

目的 研究miR-133b在胃癌细胞、正常胃黏膜上皮永生化细胞、胃癌组织及相应癌旁组织中的表达,探讨miRNA对胃癌发生发展的调控作用。方法 培养7种胃癌细胞株及正常胃黏膜上皮细胞,并收集56例胃癌患者癌组织及相应癌旁组织,提取细胞及组织中总的Small RNA,采用real-timePCR法检测miR-133b在胃癌细胞及组织中的表达,分析miR-133b的表达与细胞分化程度、临床病理特征的关系。结果 miR-133b在胃癌细胞及组织中均表达下调,差异具有统计学意义。miR-133b的低表达与细胞分化程度、TNM分期及有无淋巴结转移显著相关。结论 miR-133b在胃癌细胞及胃癌组织中的表达明显下调,可能作为抑癌基因参与胃癌的发生、发展。     

miR-200b通过靶向PROM1抑制胶质瘤细胞侵袭

目的 探讨miR-200b靶向调控PROM1的表达对胶质瘤细胞侵袭能力的影响以及miR-200b抑瘤的分子机制.方法 构建PROM1 3’端非翻译区(3'UTR)荧光素酶报告载体,荧光素酶报告检测miR-200b对PROM1 3'UTR-荧光素酶活性的影响.将miR-200b模拟物转染胶质瘤U87细胞,采用实时荧光定量PCR和Western blot检测PROM1 mRNA和蛋白的表达水平.将PROM1 siRNA转染U87细胞,Transwell侵袭实验检测PROM1下调对U87细胞侵袭能力的影响.结果 双荧光素酶报告检测显示,miR-200b能特异性地与PROM1 3'UTR结合,抑制其荧光素酶活性,其荧光素酶活性强度下降了57.0％,差异有统计学意义(P＜0.01).过表达miR-200b的U87细胞中PROM1蛋白和mRNA表达水平均降低,转染miR-200b组和对照组中PROM1 mRNA的表达水平分别为0.64 ±0.05和0.95 ±0.09,差异有统计学意义(P＜0.05).siRNA于扰PROM1表达能抑制U87细胞的生长和侵袭能力.转染PROM1siRNA组和对照组中穿膜细胞数分别为(85±9)个和(155±16)个,差异有统计学意义(P＜0.05).结论 miR-200b可通过靶向调控PROM1的表达而抑制胶质瘤细胞的侵袭力.     

HMGB1在脑胶质瘤中的表达及其对胶质瘤细胞生物学功能的影响

目的:检测高迁移率族蛋白1(high mobility group box-1,HMGB1)在胶质瘤组织和细胞中的表达情况,了解HMGB1对胶质瘤细胞增殖、侵袭迁移以及细胞周期的影响。方法:将HMGB1 siRNA真核表达质粒在脂质体介导下转染胶质瘤细胞U373、U87（HMGB1 siRNA组）,以转染无关序列siRNA质粒的细胞（negative control,NC）和未转染的胶质瘤细胞（Control,Con）作为对照。采用RT-PCR和Western blot检测HMGB1 mRNA和蛋白表达,通过CCK-8实验、Transwell实验和细胞划痕实验分别检测胶质瘤细胞增殖、侵袭和迁移能力,用流式细胞仪检测胶质瘤细胞周期的变化。结果:HMGB1 mRNA在胶质瘤组织和细胞水平上都较非肿瘤性脑组织和正常胶质细胞明显高表达,差异有统计学意义（P＜0.05）,CCK-8和划痕实验提示HMGB1 siRNA组细胞增殖和迁移能力受到明显抑制（P＜0.05）,Transwell实验显示HMGB1 siRNA组穿膜侵袭到基质胶的细胞数明显低于Con组和NC组,细胞侵袭能力减弱（P＜0.05）,流式细胞分析提示HMGB1 siRNA组位于S期细胞比例较Con和NC组明显减少（P＜0.05）,提示细胞周期发生S期阻滞。结论:应用RNAi能有效抑制HMGB1基因表达,HMGB1低表达后能抑制胶质瘤细胞增殖、侵袭和迁移,并使得细胞周期中进入S期的细胞比例明显减少,细胞周期发生阻滞,这可能为胶质瘤的基因治疗提供了新思路。     

MiR-34b和miR-155在非小细胞肺癌中的表达及临床意义

目的:检测肺癌组织及癌旁正常组织中miR-34b和miR-155的表达水平及其与肺癌临床病理特征之间的关系。方法:收集50例非小细胞肺癌患者的肺癌组织和癌旁正常肺组织标本,运用 Real-time PCR检测 miR-34b和miR-155在肺癌组织和癌旁正常肺组织中的表达情况,分析其表达与肺癌临床病理特征之间的关系。结果:Real-time PCR 检测显示在50例非小细胞肺癌组织中 miR-34b的表达显著低于癌旁正常肺组织(P=0.019),而miR-155的表达显著高于癌旁正常肺组织(P=0.000)。MiR-34b和miR-155的表达与淋巴结转移情况显著相关（P均＜0.05,miR-34b呈负相关,miR-155呈正相关）;与性别、年龄、病理类型及肿瘤分化程度无明显相关;miR-34b的表达与临床病理分期无显著相关,而miR-155表达与临床病理分期显著相关。结论:MiR-34b和miR-155的异常表达与非小细胞肺癌的发生发展相关,其可能成为肺癌的筛查、诊断及治疗的肿瘤标志物。     

血清miR-27b、miR-223水平与骨肉瘤患者化疗效果的相关性

目的:观察骨肉瘤患者血清微小RNA-27b、miR-223水平与化疗效果的相关性,指导未来临床对骨肉瘤患者实施合理的化疗。方法:选择我院2016年01月至2020年01月收治的241例骨肉瘤患者作为研究对象,均于化疗前检测血清miR-27b及miR-223水平,实施化疗治疗,分析血清miR-27b及miR-223水平与化疗效果的相关性。结果:241例骨肉瘤患者行化疗治疗后,总缓解率为59.75%;化疗后未缓解组肿瘤直径≥5 cm占比高于缓解组,化疗前血清miR-27b相对表达量高于缓解组,miR-223相对表达量低于缓解组,差异有统计学意义（P＜0.05）;两组其他基线资料比较,差异无统计学意义（P＞0.05）;经二元Logistic回归分析后建立多元回归模型,结果显示,骨肉瘤患者肿瘤直径、化疗前血清miR-27b及miR-223表达水平是化疗后未缓解的影响因素（OR＞1,P＜0.05）;绘制受试者工作曲线（ROC）发现,化疗前血清miR-27b及miR-223水平预测化疗后未缓解的曲线下面积（area under curve,AUC）均＞0.80,有一定预测性能。结论:骨肉瘤患者血清miR-27b、miR-223水平与化疗效果存在密切相关,化疗前血清miR-27b过表达及miR-223表达下调均可能提示化疗效果不佳,可将二者作为骨肉瘤患者化疗效果的有效预测因子,并根据评估结果合理调整治疗方案,可能对提高化疗整体获益意义重大。     

Down Regulated Expression Levels of miR-27b and miR-451a as a Potential Biomarker for Triple Negative Breast Cancer Patients Undergoing TAC Chemotherapy

Background: Triple negative breast cancer (TNBC) is associated with poor prognosis, aggressive phenotype(s) of tumours, partial chemotherapy response, and lack of clinically proven therapies. MicroRNAs (miRNAs) can target and modulate key genes that are involved in TNBC chemotherapy. Deregulated miRNA expression is highly involved in anti-cancer drug resistance phenotype and thus, miRNAs tend to be promising candidates for prediction of chemotherapy response and recurrence. Aim: This study aimed to investigate the expression levels of selected miRNAs (miR-21, miR-27b, miR-34a, miR-182, miR-200c and miR-451a) in cancerous and normal adjacent tissues of TNBC patients and to correlate with the clinicopathological data. Methods: Forty-one (41) FFPE tissue block of histopathologically confirmed TNBC patients was collected. Total RNA from the cancerous and adjacent non-cancerous tissues were isolated, transcribed, and pre-amplified. The relative expression level of miRNAs in tumour and normal adjacent tissues of TNBC patients was analysed using qRT-PCR. Results: Out of six miRNAs studied, the relative expression of miR-27b and miR-451a were found to be significantly lower in cancerous as compared to normal adjacent tissues of TNBC patients. In addition, a significant down regulation of miR-451a was also observed in infiltrating ductal carcinoma subtype, stages I and II, in both grade II and III, premenopausal and postmenopausal as well as in those with positive axillary lymph node metastases. Conclusion: The results suggest the possible utilization of miR-27b and miR-451a expression levels as potential predictive risk markers for TNBC patients undergoing TAC chemotherapy.     

12-LOX在神经胶质瘤中的表达及临床意义*

目的：研究12- 脂氧合酶（12-lipoxygenase ,12-LOX）在神经胶质瘤中的表达及其临床意义。方法：免疫组织化学法检测40例神经胶质瘤组织和10例正常脑组织中12-LOX 表达,结合临床随访资料探讨其表达与预后的相关性。结果：正常脑组织中12-LOX 呈弱阳性表达,神经胶质瘤组织中强阳性表达率为72.5% ,差异有统计学意义（P < 0.05）。 12-LOX 强阳性表达与神经胶质瘤病理级别相关,差异有统计学意义（P = 0.012）,与患者性别、年龄、肿瘤大小、KPS 评分无关。12-LOX 强阳性表达患者中位无瘤生存期明显低于与弱阳性表达患者（P < 0.05）。 结论：12-LOX 在神经胶质瘤中异常表达,其表达差异与神经胶质瘤的病理级别相关,与预后密切相关。     

胶质瘤组织中miR-205-5p的表达及其对胶质瘤细胞恶性生物学行为的影响

目的 探讨miR-205-5p在胶质瘤中的表达以及对胶质瘤细胞增殖、迁移和侵袭的调控及可能的作用机制。方法 收集2018 年6 月至2019 年12 月于郴州市第一人民医院诊治的58 例新发神经胶质瘤患者的胶质瘤组织和癌旁组织标本。将miR-205-5p mimic转染至U251和T98G细胞,构建过表达细胞模型。采用RT-qPCR检测胶质瘤组织及细胞模型中miR-205-5p的表达水平并分析其表达水平与患者临床病理特征的关系,CCK-8法、平板克隆形成实验、划痕实验和Transwell小室实验分别检测胶质瘤细胞的增殖、克隆形成、迁移和侵袭情况,Western blot检测过表达miR-205-5p对Runt相关因子2（runt-related gene 2,Runx2）蛋白表达水平的影响;用双荧光素酶报告基因实验检测miR-205-5p与Runx2的靶向关系。结果 miR-205-5p在胶质瘤组织和胶质瘤细胞U251和T98G中低表达（均P＜0.01）,其表达水平与肿瘤大小和病理分级有关（均P＜0.05）。过表达miR-205-5p可以显著抑制胶质瘤细胞增殖、克隆形成、迁移和侵袭能力（均P＜0.05）。双荧光素酶报告实验证实Runx2基因是miR-205-5p的潜在靶基因。过表达miR-205-5p可明显下调胶质瘤细胞中Runx2蛋白的表达水平（P＜0.001）。结论 miR-205-5p在胶质瘤中低表达,过表达miR-205-5p可抑制胶质瘤细胞增殖、克隆形成、迁移和侵袭,作用机制可能与靶向调控Runx2有关。     

miR-30b对结直肠癌细胞转移潜能的影响

  目的   明确miR-30b对结直肠癌细胞侵袭和迁移潜能的影响。   方法   RT-qPCR检测20对配对结直肠癌组织标本中miR-30b的表达;Transwell和划痕实验检测过表达和抑制miR-30b后结直肠癌细胞侵袭和迁移潜能的改变;应用生物信息学方法预测miR-30b的作用靶点;Western Blot及双荧光素酶报告基因实验验证过表达和抑制miR-30b后靶点Snail和EMT（epithelial mesenchymal transition）标志物的表达情况。   结果   癌组织中miR-30b表达水平明显低于正常肠黏膜组织;Transwell及划痕实验结果显示过表达miR-30b后结直肠癌细胞的侵袭迁移能力降低,抑制miR-30b后侵袭迁移能力增强;生物信息学预测结果显示miR-30b能够作用于Snail 3'-UTR,双荧光素酶检测结果进一步证实miR-30b能够作用于Snail 3'-UTR;Western Blot结果显示过表达miR-30b后Snail的表达下降,EMT标志物Vimentin表达下降和E-cadherin表达升高,而抑制miR-30b后结果相反。   结论   miR-30b在结直肠癌中表达水平下降,并通过靶向Snail调节结直肠癌细胞的侵袭和迁移。