血清微小RNA(miR-129-3p、miR-767-3p和miR-877)在结直肠癌诊断中的价值

目的:探讨血清微小RNA (microRNA,mi RNA)在结直肠癌诊断中的价值.方法:通过miRNA表达谱芯片检测7例结直肠癌患者血清和10例健康志愿者血清中差异表达的miRNA.应用实时荧光定量PCR法在40例结直肠癌患者血清和18例健康志愿者血清中验证芯片结果,并分析血清特异性miRNA在结直肠癌诊断中的价值.结果:筛选获得10个在结直肠癌中特异性表达的血清miRNA,实时荧光定量PCR验证后获得一组结直肠癌特异性血清miRNA(miR-129-3p、miR-767-3p及miR-877*)生物标志物,这组生物标志物组合检测结直肠癌的灵敏度为77.78％、特异度为100％,并可产生最大受试者工作特征曲线(receiver operator characteristic curve,ROC)的曲线下面积(area under the curve,AUC)为0.914.结论:miR-129-3p、miR-767-3p和miR-877*生物标志物组合有望成为结直肠癌筛查和早期诊断的指标.     

Associations of Single Nucleotide Polymorphisms in miR-146a,miR-196a,miR-149 and miR-499 with Colorectal Cancer Susceptibility

Background: MicroRNAs (miRNAs) are an abundant class of endogenous small non-coding RNAs of 20-25nucleotides in length that function as negative gene regulators. MiRNAs play roles in most biological processes,as well as diverse human diseases including cancer. Recently, many studies investigated the association betweenSNPs in miR-146a rs2910164, miR-196a2 rs11614913, miR-149 rs229283, miR-499 rs3746444 and colorectalcancer (CRC), which results have been inconclusive. Methodology/Principal Findings: PubMed, EMBASE,CNKI databases were searched with the last search updated on November 5, 2013. For miR-196a2 rs11614913,a significantly decreased risk of CRC development was observed under three genetic models (dominant model:OR = 0.848, 95%CI: 0.735–0.979, P = 0.025; recessive model: OR = 0.838, 95%CI: 0.721–0.974, P = 0.021;homozygous model: OR = 0.754, 95%CI: 0.627–0.907, P = 0.003). In the subgroup analyses, miR-196a2*Tvariant was associated with a significantly decreased susceptibility of CRC (allele model: OR = 0.839, 95%CI:0.749–0.940, P = 0.000; dominant model: OR = 0.770, 95%CI: 0.653–0.980, P = 0.002; recessive model: OR =0.802, 95%CI: 0.685–0.939, P = 0.006; homozygous model: OR = 0.695, 95%CI: 0.570–0.847, P = 0.000). Asfor miR-149 rs2292832, the two genetic models (recessive model: OR = 1.199, 95% CI 1.028-1.398, P = 0.021;heterozygous model: OR = 1.226, 95% CI 1.039-1.447, P = 0.013) demonstrated increased susceptibility to CRC.On subgroup analysis, significantly increased susceptibility of CRC was found in the genetic models (recessivemodel: OR = 1.180, 95% CI 1.008-1.382, P = 0.040; heterozygous model: OR = 1.202, 95% CI 1.013-1.425, P =0.013) in the Asian group. Conclusions: These findings supported that the miR-196a2 rs11614913 and miR-149rs2292832 polymorphisms may contribute to susceptibility to CRC.     

Clinical Potentials of miR-576-3p,miR-613, NDRG2 and YKL40 in Colorectal Cancer Patients

Introduction: Colorectal cancer (CRC) is the most common type of gastrointestinal tract cancers. This investigation aim was to assess the expression of miR-576-3p and miR-613 in CRC patients in addition to NDRG2 and YKL40 serum levels determination to decide their diagnostic and prognostic significance. Methods: Sixty early diagnosed CRC patients prior to any treatment in addition to twelve healthy subjects were enrolled in this study. Blood samples were taken from subjects and allowed for clotting and centrifugation, then the collected sera were stored at -80ºC till it were used for detection of our molecular biomarkers. The mature miRNAs expressions (miR-576-3p and miR-613) were detected in serum by qRT-PCR, while NDRG2 and YKL40 serum levels were determined by ELISA. In addition, the correlation of the measured parameters with the clinicopathological data of the patients was investigated. Results: The study results showed that both miRNA-576-3p and miRNA-613 were down-regulated in CRC patients with fold change 0.33, 0.36; respectively. A significant positive correlation was observed between miR-576-3p and miR-613 (r = 0.75, p < 0.001). NDRG2 serum levels were decreased in patients compared to the control group but the decrease wasn’t statistically significant. On the other hand, it was observed that YKL40 serum level was significantly increased in CRC patients compared to control (p-value < 0.001). Furthermore, YKL40 showed a very high diagnostic value (AUC = 0.97, specificity = 91.7%, sensitivity = 96%, p-value = 0.0001). Conclusion: The observations of this investigation concluded that, the expressions of miR-576-3p and miR-613 in addition to YKL40 serum levels determinations may help in the diagnosis of CRC.     

miR-489抑制结直肠癌细胞的侵袭转移

目的:探究miR-489在结直肠癌(colorectal cancer,CRC)中的表达情况及其临床意义,并进一步探究miR-489对CRC细胞的侵袭迁移的作用.方法:应用Real-time PCR检测miR-489在CRC组织和细胞系中的表达情况;分析miR-489与CRC临床病理特征的关系;应用Transwell实验探究miR-489对CRC细胞的侵袭与迁移能力的影响;Western blot探究miR-489对CRC细胞上皮-间质转化(epithelial to mesenchymal transition,EMT)的作用.结果:Real-time PCR结果显示miR-489在CRC组织和细胞系中均为显著性低表达(P＜0.05);统计学分析显示miR-489的表达量与CRC的静脉浸润、浸润深度以及淋巴结转移呈显著相关(P＜0.05);Transwell实验结果显示miR-489能够抑制CRC细胞的侵袭与迁移;Western blot结果显示miR-489能够抑制CRC细胞的EMT.结论:miR-489在CRC中为低表达,其能够通过抑制CRC细胞的侵袭、迁移与EMT发挥其抗CRC作用.     

Serum miR-21 and miR-92a as biomarkers in the diagnosis and prognosis of colorectal cancer

Previous studies from our laboratory identified a number of miRNAs that were aberrantly expressed in colorectal cancer (CRC) tissue. However, their diagnostic and prognostic value in serum has not been fully evaluated. In the present study, we measured the levels of five miRNAs (miR-21, miR-31, miR-92a, miR-18a, and miR-106a) in serum samples from 200 CRC patients, 50 advanced adenoma patients, and 80 healthy controls by real-time quantitative polymerase chain reaction (RT-PCR). In our study, the levels of miR-21 and miR-92a in patients with CRC and advanced adenoma were significantly higher than those in healthy controls (all P?<?0.05). MiR-21 yielded an area under the receiver-operating characteristics (ROC) curve (AUC) of 0.802 and miR-92a yielded an AUC of 0.786 in discriminating CRCs from the controls. Additionally, miR-21 and miR-92a yielded an AUC of 0.709 and 0.701, respectively, in discriminating advanced adenomas from the controls. Combined ROC analyses using both miRNAs, revealed an elevated AUC of 0.847 in discriminating CRCs, and an AUC of 0.722 in discriminating advanced adenomas from the controls. In the multivariate Cox proportional hazards analysis, high miR-92a expression in CRC was independently associated with poor survival (P?=?0.03; hazard ratio 4.36; 95 % confidence interval?=?1.64–11.57). No significant difference was observed in the levels of miR-18a, miR-31, and miR-106a among CRC, advanced adenoma, and control samples. In summary, our data indicate that miR-21 and miR-92a serum levels have potential value for early detection of CRC. Furthermore, miR-92a has prognostic value in CRC patients.     

Clinical and biological significance of miR-378a-3p and miR-378a-5p in colorectal cancer

To investigate miR-378a-3p and miR-378a-5p expression and their relationships with the clinicopathological features of colorectal cancer (CRC). Our results showed that miR-378a-3p and miR-378a-5p expression were dramatically lower in CRC cell lines and tissues than that in adjacent normal colorectal mucosal tissues, respectively. MiR-378a-3p and miR-378a-5p expression were significantly associated with histological differentiation and TNM stage, respectively. CRC patients with low miR-378a-3p and miR-378a-5p expression had a significantly shorter survival time than those patients with high miR-378a-3p and miR-378a-5p expression (p < 0.001, p < 0.001), respectively. Univariate and multivariable Cox regression analysis showed that tumour size, TNM stage, miR-378a-3p expression and miR-378a-5p expression were independent prognostic factors for CRC patients. Ectopic miR-378a-3p or miR-378a-5p expression inhibited cellular proliferation and colony formation, induced apoptosis and G1-phase cell cycle arrest in CRC cells, but had no effect on migration and invasion of CRC cells. Furthermore, miR-378a-3p over-expression or down-regulation could inhibit or enhance insulin-like growth factor 1 receptor (IGF1R) expression in CRC cells. There was a significantly negative correlation between IGF1R protein expression and miR-378a-3p expression in CRC tissues. MiR-378a-3p over-expression or down-regulation suppressed or enhanced phosphorylated-ERK1/2 protein level, but had no effect on phosphorylated-Akt protein level. In conclusion, miR-378a-3p and miR-378a-5p expression might play an important role as tumour suppressor gene in the initial stage of carcinogenesis of CRC.     

Differential expression of serum miR-126,miR-141 and miR-21 as novel biomarkers for early detection of liver metastasis in colorectal cancer简

Objective：MicroRNAs （miRNAs） have potential as diagnostic biomarkers in cancer.Evaluation of the association between miRNA expression patterns and early detection of liver metastasis in colorectal cancer （CRC） has not been reported.Methods：We investigated the expression of metastasis-associated miRs-31,335,206,141,126,200b,200c,21,Let7a,Let7b and Let7c in localized,liver-metastatic and other organ-metastatic CRC （OM-CRC）.Expressions of target miRNAs in serum were evaluated in 116 consecutive localized CRC （L-CRC）,72 synchronous liver-metastatic CRC （SLM-CRC） and 36 other OM-CRC by quantitative real-time PCR.Results：Seven of 11 tested miRNAs could be detected from serum.Four miRNAs,miR-126,Let-7a,miR141 and miR-21 were identified as metastasis-associated miRNAs.Compared with L-CRC,significant upregulated expression was observed for miR-141 and miR-21 in SLM-CRC and OM-CRC,down-regulated expression was observed for miR-126 in SLM-CRC and OM-CRC,and up-regulated expression of Let-7a in OM-CRC.The receiver operating characteristic （ROC） curve showed serum miR-126 had a cut-off [log10 relative quantity （log10RQ）=--0.2005] with 77.78％ sensitivity and 68.97％ specificity with an area under curve （AUC） of 0.7564,miR-141 had a cut-off （1og10RQ=-0.2285） with 86.11％ sensitivity and 76.11％ specificity with an AUC of 0.8279,and miR-21 had a cut-off （log10RQ=-0.1310） with 73.61％ sensitivity and 66.38％ specificity with an AUC of 0.7479.Conclusions：We identified liver metastasis-associated miRNAs,suggesting serum miR-126,miR-141 and miR-21 may be novel biomarkers for clinical diagnosis of early stage liver-metastatic CRC.     

Silencing of miR-1-1 and miR-133a-2 cluster expression by DNA hypermethylation in colorectal cancer

MicroRNAs are small non-coding RNA molecules that play important roles in the multistep process of colorectal carcinoma (CRC) development. The present study evaluated the relationship between miR-1-1 and miR-133a-2 expression and DNA methylation, and its putative biological role in CRC. The results indicated that DNA methylation regulated the expression of the miR-1-1 and miR-133a-2 cluster in CRC cell lines. Expression of miR-1 and miR-133a was further evaluated in 64 paired tissue samples (CRC tumor and adjacent normal mucosa) using the stem-loop real-time polymerase chain reaction. The miR-1-133a cluster displayed significantly lower expression in CRC tissue compared to adjacent normal mucosa (P<0.001). The results also indicated frequent hypermethylation of the CpG islands upstream of miR-1-133a (54.6%). Liver metastatic tissues exhibited significantly lower miR-1 (P<0.001) and miR-133a (P<0.001) expression compared to adjacent normal mucosa. Expression of the miR-1-133a cluster inversely correlated with TAGLN2 in the tumor specimens. In conclusion, epigenetic repression of the miR-1-133a cluster may play a critical role in colorectal cancer metastasis by silencing TAGLN2.     

血清中miR-29a和miR-92a在结直肠癌诊断和预后判断中的价值

目的探讨血清微小RNA（miR-29a和miR-92a）在结直肠癌（CRC）诊断和预后判断中的价值。方法选取无转移的结直肠癌患者50例和存在肝转移的患者48例,同时募集50名健康志愿者为对照组,按类似的年龄和性别相匹配的队列组合。应用实时荧光定量聚合酶链反应（PCR）法检测微小RNA（miR-29a和miR-92a）水平,判断该血清微小RNA在结直肠癌早期诊断和预后判断中的价值。结果结直肠癌患者血清中miR-29a和miR-92a水平均显著高于健康对照者（P〈0.01）;血清miR-29a和miR-92a分别进行结直肠癌诊断时的灵敏度为71.4%和75.3%,特异度为84.0%和88.3%;结直肠癌肝转移患者血清中miR-29a和miR-92a水平均显著高于未转移的CRC患者（P〈0.05）;miR-29a和miR-92a分别鉴别转移性与非转移性CRC患者的敏感性为79.4%和78.6%,特异性为85.3%和86.6%。结论 miR-29a和miR-92a可能是新的非侵入性指标用于结直肠癌患者的早期诊断,血清中miR-29a和miR-92a水平升高与结直肠癌患者预后有关,miR-29a和miR-92a有望成为结直肠癌筛查和早期诊断和预后判断的指标。     

miR-106b enhances cell radioresistance by targeting PTEN in colorectal carcinoma

Objective To investigate the role of miR-106b in the cell radioresistance in colorectal carcinoma (CRC), and unravel the underlying mechanism. Methods The CRC cell lines stably overexpressing and interfering miR-106b were established. The effect of miR-106b upon the CRC cell radiosensitivity was evaluated by cell radiation, immunofluorescence and colony formation assay. The expression levels of Caspase-3 and γ-H2AX were detected by Western blot. The target genes of miR-106b were identified by bioinformatics prediction, which were further validated by dual luciferase assay, fluorescence quantitative PCR and Western blot. The CRC cell lines stably overexpressing miR-106b were transfected with pCDNA3.0-PTEN. The changes of CRC cell radiosensitivity were investigated. Whether miR-106b could increase the radioresistance of CRC cells by targeting PTEN was clarified. Results Compared with the control group (miR-ctr group), the cell surviving fraction was significantly elevated (P<0.05), the radioresistance (P<0.05) was considerably enhanced and the expression levels of Caspase-3 and γ-H2AX were significantly down-regulated (both P<0.05) in the miR-106b overexpression group. PTEN up-regulation in CRC cell lines stably overexpressing miR-106b could reverse the radioresistance induced by miR-106b. Conclusion miR-106b can induce CRC cell radioresistance by inhibiting PTEN, prompting that miR-106b-PTEN might provide theoretical evidence for relevant targets which can enhance the clinical efficacy of radiotherapy.     

miR-106b靶向调控PTEN促进结直肠癌细胞放射抵抗

目的 阐明miR-106b在结直肠癌细胞放射敏感性中的作用及机制。方法 构建稳定过表达和干扰miR-106b结直肠癌细胞系,通过免疫荧光和平板克隆实验探讨miR-106b对结直肠癌细胞放射敏感性的影响;Western blot检测Caspase-3和γ-H2AX的表达;生物信息学预测miR-106b下游调控的靶基因,双荧光素酶报告系统、荧光定量PCR及Western blot进一步验证。在稳定过表达miR-106b的结直肠癌细胞系中转染pCDNA3.0-PTEN,探讨细胞放射敏感性变化,明确miR-106b是否通过靶向调控PTEN增加结直肠癌细胞放射抵抗。结果 在结直肠癌细胞系过表达miR-106b,经过同等条件的照射处理后,与对照组相比,过表达miR-106b组细胞存活分数升高,放射抵抗增强(P<0.05),Caspase-3及γ-H2AX表达降低。在稳定过表达miR-106b的细胞中上调PTEN后能逆转miR-106b引起的放射抵抗。结论 miR-106b通过靶向抑制PTEN从而诱导结直肠癌细胞放射抵抗,预示着miR-106b-PTEN位点可能为临床提高结直肠癌放疗效果寻找相关靶点提供理论依据。     

miR-455 Functions as a Tumor Suppressor Through Targeting GATA6 in Colorectal Cancer

Emerging evidence indicates that microRNAs (miRNAs) are often aberrantly expressed in human cancers. Meanwhile, the importance of miRNAs in regulating multiple cellular biological processes has been appreciated. The aim of this study was to investigate the significance of miR-455 and identify its possible mechanism in regulating colorectal cancer (CRC) progression. We found that the expression of miR-455 was sharply reduced in CRC tissues and cell lines. Importantly, the low expression of miR-455 was associated with poor overall survival of CRC patients. Overexpression of miR-455 in CRC cell lines significantly inhibited cell proliferation and migration in vitro. Moreover, GATA-binding protein 6 (GATA6), whose expression can be inversely regulated by miR-455 in CRC cell lines, was validated as a direct target of miR-455. Overall, our results revealed that miR-455 functions as a tumor suppressor, and its downregulation may contribute to CRC progression. Our study may provide a novel therapeutic target for CRC in the future.     

miR-124 and miR-506 inhibit colorectal cancer progression by targeting DNMT3B and DNMT1

miR-124 and miR-506 are reportedly down-regulated and associated with tumor progression in many cancers, but little is known about their intrinsic regulatory mechanisms in colorectal cancer (CRC). In this study, we found that the miR-124 and miR-506 levels were significantly lower in human CRC tissues than in controls, as indicated by qRT-PCR and in situ hybridization histochemistry. We also found that the overexpression of miR-124 or miR-506 inhibited tumor cell progression and increased sensitivity to chemotherapy in vitro. Increased miR-124 or miR-506 expression also inhibited tumor cell proliferation and invasion in vivo. Luciferase reporter assays and western blotting were used to determine the association between miR-124, miR-506 and their target genes, DNMTs. We further identified that miR-124 and miR-506 directly targeted DNMT3B and indirectly targeted DNMT1. The overexpression of miR-124 and miR-506 reduced global DNA methylation and restored the expression of E-cadherin, MGMT and P16. In conclusion, our data showed that miR-124 and miR-506 inhibit progression and increase sensitivity to chemotherapy by targeting DNMT3B and DNMT1 in CRC. These findings may provide novel avenues for the development of targeted therapies.     

miR-92a 在结直肠癌中的表达及其对肿瘤血管生成的作用*

目的:探讨miR-92a 在结直肠癌中的表达及其对肿瘤血管新生功能的影响和作用机制。方法:采用qRT-PCR方法检测广东医学院附属深圳南山医院2014年6 月至2015年12月经手术切除的25例结直肠癌组织和对应癌旁组织及4 种结直肠癌细胞（HCT 116、SW620、SW480、HT29）中miR-92a 的表达;免疫组织化学法检测结直肠癌和癌旁组织中CD31阳性表达的微血管密度（microvesseldensity,MVD）,Pearson相关性分析探讨miR-92a 表达与肿瘤血管新生MVD的相关性。通过转染miR-92a-mimic、inhibitor 上调或抑制结直肠癌细胞HCT 116、SW620 中miR-92a 的表达水平,采用小管形成实验检测miR-92a 不同表达对HUVEC小管形成的影响,免疫印迹法检测对其下游潜在靶点PTEN的蛋白表达的影响。结果:结直肠癌组织miR-92a 的表达水平显著高于对应癌旁组织（P < 0.01）;4 种人结肠癌细胞系miR-92a 的表达水平均显著高于正常肠上皮组织（P < 0.05）;结直肠癌组织CD31阳性微血管密度显著高于癌旁组织（P < 0.01）,miR-92a 表达水平与结直肠癌血管新生MVD呈显著正相关（r = 0.580,P = 0.01）;上调miR-92a 表达的HCT 116 细胞培养上清液可以显著促进HUVEC小管形成（P < 0.05）;上调miR-92a 表达可以显著抑制HCT116 细胞中PTEN蛋白表达水平（P < 0.01）。 结论:miR-92a 在结直肠癌细胞和组织中高表达,与肿瘤血管新生增加密切相关;miR-92a 可能通过抑制PTEN的表达发挥促进结直肠癌血管新生的生物学功能。      

miR-302a对结直肠癌细胞奥沙利铂化疗敏感性的影响及机制

目的:探究miR-302a对结直肠癌细胞奥沙利铂化疗敏感性的影响及机制。方法:在四株结直肠癌细胞系HT29、HCT8、SW480、SW1463中,通过转染miR-302a mimic构建miR-302a过表达模型,RT-PCR检测过表达效果;CCK-8法检测转染48 h后高表达miR-302a细胞的增殖能力及对奥沙利铂的敏感性;蛋白质印迹法检测转染后P-gp蛋白及Wnt/β-catenin通路相关蛋白MMP-7、c-Jun、c-myc、β-catenin、LEF1的变化。结果:相比正常小肠上皮细胞HIEC,miR-302a在结直肠癌细胞系HT29、HCT8、SW480、SW1463中的表达较低。转染mimic后,miR-302a的表达明显上调（P<0.001）。增殖实验发现miR-302a的上调并不影响结直肠癌细胞的增殖,而在转染miR-302a的细胞中加入奥沙利铂,miR-302a组HT29、HCT8、SW480和SW1463细胞存活率相比miR-NC组分别降低2.46、1.89、2.39、2.86倍。进一步探究miR-302a增加奥沙利铂敏感性的机制,发现miR-302a可抑制P-gp蛋白的表达,并且抑制Wnt/β-catenin通路相关蛋白MMP-7、c-Jun、c-myc、β-catenin、LEF1的表达。结论:miR-302a可增加结直肠癌细胞奥沙利铂化疗敏感性,其机制可能是通过抑制P-gp的蛋白表达,并抑制Wnt/β-catenin信号通路相关蛋白表达而实现。     

Circulating miR-182 is a biomarker of colorectal adenocarcinoma progression

MiR-182 expression was evaluated by qRT-PCR and in situ hybridization in 20 tubular adenomas, 50 colorectal carcinoma (CRC), and 40 CRC liver metastases. Control samples obtained from patients with irritable bowel syndrome, or tumor-matched normal colon mucosa were analyzed (n=50). MiR-182 expression increased progressively and significantly along with the colorectal carcinogenesis cascade, and in CRC liver metastases. The inverse relation between miR-182 and the expression of its target gene ENTPD5 was investigated by immunohistochemical analysis. We observed that normal colocytes featured a strong ENTPD5 cytoplasmic expression whereas a significantly and progressively lower expression was present along with dedifferentiation of the histologic phenotype. Plasma samples from 51 CRC patients and controls were tested for miR-182 expression. Plasma miR-182 concentrations were significantly higher in CRC patients than in healthy controls or patients with colon polyps at endoscopy. Moreover, miR-182 plasma levels were significantly reduced in post-operative samples after radical hepatic metastasectomy compared to preoperative samples. Our results strengthen the hypothesis of a central role of miR-182 dysregulation in colon mucosa transformation, demonstrate the concomitant progressive down-regulation of ENTPD5 levels during colon carcinogenesis, and indicate the potential of circulating miR-182 as blood based biomarker for screening and monitoring CRC during the follow-up.     

miR-17 在结肠癌中的表达及其临床意义

目的探讨miR-17在结肠癌中的表达与临床病理特征间的关系。方法选取2012年1月至2013年6月经手术切除的50例原发性结肠癌及癌旁组织标本,采用实时荧光定量PCR分析miR-17的表达情况。结果相对于癌旁组织,50例结肠癌组织中miR-17表达下调(P<0.05),其表达与TNM分期以及浸润深度有关(均P<0.05)。结论 miR-17参与了结肠癌的发生发展。     

miR-21 functionally interacts with the 3'UTR of chemokine CCL20 and down-regulates CCL20 expression in miR-21 transfected colorectal cancer cells

As deregulation of miRNAs and chemokine CCL20 was shown to play a role in colorectal cancer (CRC) pathogenesis, we analyzed the functional interactions of candidate miRNAs with CCL20 mRNA. After target prediction software programs indicated a role for miR-21 in CCL20 regulation, we applied the luciferase reporter assay system to demonstrate that miR-21 functionally interacts with the 3′UTR of CCL20 mRNA and down-regulates CCL20 in miR-21 mimic transfected CRC cell lines (Caco-2, SW480 and SW620). Thus, regulation of CCL20 expression by miR-21 might be a regulatory mechanism involved in progression of CRC.     

LncRNA SNHG5 affects cell proliferation,metastasis and migration of colorectal cancer through regulating miR-132-3p/CREB5

We aimed at the effects of long non-coding RNA (lncRNA) SNHG5 on proliferation, metastasis and migration of colorectal cancer (CRC) cells. We also investigated regulatory relationships among miR-132-3p, SNHG5 and CREB5 and their roles in CRC. 25 pairs of samples containing CRC tissues and matched para-tumor tissues were obtained to examine SNHG5, miR-132-3p and CREB5 expression by qRT-PCR or Western blot. The targeted relationship between miR-132-3p and SNHG5 or CREB5 was confirmed by dual luciferase report assay as well as RNA pull down assay. The expression of SNHG5, miR-132-3p and CREB5 in CRC cells were regulated by cell transfection. CRC cellular proliferation was assayed by CCK-8 and meanwhile flow cytometry was adopted to observe apoptosis. Metastasis and migration of CRC cells were determined respectively by means of Transwell assay and scratch test. The effects of SNHG5 on CRC were researched in vivo, too. SNHG5 or CREB5 was up-regulated in CRC tissues and cells, whereas miR-132-3p was down-regulated. Overexpression of SNHG5 and CREB5 resulted in the enhancement of proliferation, metastasis, migration and the inhibition of apoptosis in CRC cells, while miR-132-3p led to the opposite result. LncRNA SNHG5 promoted proliferation, migration and metastasis of CRC cells but inhibited apoptosis by modulating miR-132-3p/CERB5.