MiR-18b-5p对大肠癌PTEN/PI3K/Akt2信号通路的调控

目的:探讨miR-18b-5p对大肠癌PTEN/PI3K/Akt2信号转导通路的调控。方法:qRT-PCR方法检测33例大肠癌患者癌组织中miR-18b-5p表达水平,将患者临床病理特征与癌组织miR-18b-5p表达水平进行独立样本t检验和多元线性回归分析。应用microrna.org预测miR-18b-5p靶基因,miR-18b-5p 类似物、抑制物转染肠癌细胞SW480及HCT116,qRT-PCR检测细胞PTEN、PI3K、Akt2 mRNA表达水平。结果:在大肠癌患者癌组织中,miR-18b-5p表达水平显著增高,为癌旁组织的3.6倍(P<0.01 ),其表达水平与肿瘤分化程度、淋巴结转移及TNM分期相关。Microrna.org预测PTEN可能是miR-18b-5p的靶基因,大肠癌细胞转染类似物后PTEN含量明显降低,其下游基因PI3K、Akt2表达增高。结论:miR-18b-5p下调抑癌基因PTEN表达,诱导PI3K/Akt2信号转导通路持续活化,促进了大肠癌的发生发展。     

miR-103 靶向PTEN并激活PI3K/AKT通路促进肺癌细胞A549 对达沙替尼耐药

[摘要] 目的：探讨miR-103 靶向PTEN并激活PI3K/AKT信号通路促进肺癌细胞对达沙替尼（dasatinib,DASA）耐药的机制。方法：收集2014 年4 月至2018 年1 月昆明医科大学第一附属医院胸外科收治的资料完整的肺癌DASA耐药组织和不耐药组织各35 例。采用qPCR实验检测miR-103 在肺癌DASA耐药组织和细胞中的表达水平,同时,采用CCK-8、Transwell 和Wb实验检测敲降miR-103 对A549/DASA细胞增殖、迁移和上皮间质转化（EMT）的影响,双荧光素酶报告基因验证miR-103 与PTEN的靶向关系。进一步采用CCK-8、Transwell 和Wb实验检测miR-103 通过PTEN-PI3K/AKT信号通路对A549/DASA细胞恶性生物学行为的影响。结果：miR-103 在肺癌DASA 耐药组织和A549/DASA 细胞中均高表达（均P<0.01）。敲降miR-103 可显著抑制A549/DASA细胞的增殖、迁移和EMT（P<0.05 或P<0.01）。此外,双荧光素酶报告基因证实miR-103 靶向作用PTEN并下调其表达水平（P<0.01）。进一步实验显示,过表达miR-103 通过靶向下调PTEN并激活PI3K/AKT信号通路进而显著促进A549/DASA细胞增殖、迁移和EMT（P<0.05 或P<0.01）,从而上调A549/DASA细胞对DASA的耐药性。结论：miR-103/PTEN/PI3K/AKT信号通路与肺癌DASA耐药性存在调控关系,敲降miR-103 可逆转A549/DASA对DASA耐药。     

miR-140-5p靶向HDAC7抑制非小细胞肺癌细胞增殖、迁移和侵袭的机制探讨

目的:探讨miR-140-5p靶向组蛋白去乙酰化酶7(histone deacetylase 7,HDAC7)调控非小细胞肺癌（non-small cell lung cancer,NSCLC）细胞增殖、迁移和侵袭的机制。方法:采用qRT-PCR检测人NSCLC组织及癌旁组织中miR-140-5p的表达水平。用miR-140-5p mimic（模拟物）及miR-140-5p NC（阴性对照）转染A549细胞,CCK8法及克隆形成实验检测细胞增殖能力,划痕实验和Transwell实验检测细胞迁移和侵袭能力,双荧光素酶报告基因实验验证miR-140-5p与HDAC7的靶向关系,Western blot检测各组细胞HDAC7及PI3K、p-PI3K、AKT、和p-AKT表达水平。结果:与癌旁组织相比,miR-140-5p在NSCLC组织中的表达水平明显减低,差异有统计学意义（P＜0.01）。与miR-140-5p NC组相比,过表达miR-140-5p后A549细胞在48和72 h的增殖能力明显降低（P＜0.05）;且细胞克隆形成、细胞迁移和侵袭能力均降低（均P＜0.05）,PI3K/AKT信号通路中关键分子p-PI3K和p-AKT蛋白水平明显降低（均P＜0.05)。生物信息学预测HDAC7可能是miR-140-5p的一个靶基因,且双荧光素酶报告结果证实miR-140-5p直接靶向调节HDAC7表达。结论:miR-140-5p通过靶向HDAC7表达进而抑制NSCLC A549细胞的增殖、迁移和侵袭,其机制可能与通过抑制PI3K/AKT信号通路的激活有关。     

SP1-mediated microRNA-520d-5p suppresses tumor growth and metastasis in colorectal cancer by targeting CTHRC1

Recent evidence suggests that miR-520 family has an important role in regulating tumorigenesis and development of various types of solid cancers. However, as one of the most common cancers in the world, there is little known about the underlying regulatory mechanisms of miR-520 in colorectal cancer (CRC). In the present study, we investigated the expression of microRNA-520d-5p (miR-520d-5p) in CRC specimens and then explored its potential role and mechanism in CRC progression. We found that miR-520d-5p was markedly down-regulated in CRC clinical specimens compared with adjacent normal tissues by real-time PCR. Dual-luciferase assays confirmed that miR-520d-5p directly targeting CTHRC1 and SP1 transactivate miR-520d-5p by binding to its upstream promoter region. The biological functional experiments showed that ectopic re-expression of miR-520d-5p suppressed CRC cell proliferation, migration and invasion, whereas the inhibition of miR-520d-5p displayed an inverse effect in vitro and in vivo. Western blot shown that miR-520d-5p abrogated the epithelial-mesenchymal transition by inactivating the phosphorylation of Erk1/2. In conclusion, our findings indicate that miR-520d-5p is significantly down-expressed and involved in CRC progression and metastasis by targeting CTHRC1 and regulated by SP1, which provide new support for miR-520d-5p maybe as a novel anti-onco molecular target for the treatment of CRC in the future.     

lncRNA DLEU2/miR-455-3p/OTUD7B轴通过PI3K/AKT信号通路促进宫颈癌恶性发展

目的:探讨长链非编码RNA DLEU2(lncRNA DLEU2,DLEU2)对宫颈癌恶性发展的影响。方法:利用TCGA数据库和qRT-PCR分析DLEU2在宫颈癌组织和细胞系中的表达。采用CCK-8、Western blotting、免疫荧光、细胞划痕、Transwell和TUNEL实验检测干扰DLEU2(sh-DLEU2)对宫颈癌细胞增殖、迁移、侵袭和凋亡的影响。生物信息学和双荧光素酶报告基因实验分析DLEU2和miR-455-3p的靶基因,评估miR-455-3p inhibitor/mimic对宫颈癌细胞生长和PI3K/AKT信号通路的影响。裸鼠荷瘤实验检测干扰DLEU2后对瘤体体内生长的影响。结果:宫颈癌组织和细胞系中DLEU2表达显著上调（P＜0.01）。sh-DLEU2可抑制Hela和SiHa细胞的增殖、迁移和侵袭（P＜0.01）,促进细胞凋亡（P＜0.001）。DLEU2与miR-455-3p相结合,OTUD7B为miR-455-3p的靶基因。miR-455-3p inhibitor促进细胞恶性发展并激活PI3K/AKT信号通路,而sh-DLEU2可逆转其作用（P＜0.01）;miR-455-3p mimic也可部分逆转Oe-OTUD7B对细胞的作用（P＜0.01）。此外,sh-DLEU2抑制了裸鼠荷瘤组织的生长（P＜0.01）。结论:DLEU2通过miR-455-3p/OTUD7B轴激活PI3K/AKT信号通路促进宫颈癌的恶性发展。     

miR-429通过下调PTEN并激活PI3K/AKT信号通路促进胰腺癌PANC-1细胞对卡培他滨耐药

目的:探讨miR-429 靶向PTEN并通过PI3K/AKT信号通路调控胰腺癌PANC-1 细胞对卡培他滨的耐药性及其作用机制。方法：建立胰腺癌卡培他滨耐药细胞株PANC-1/CAP后,采用qRT-PCR和Western blotting 实验检测miR-429 和PTEN在胰腺癌细胞中的表达情况,平板克隆形成实验、CCK-8 法和Annexin V-FITC/PI 双染流式细胞术检测敲降miR-429 对胰腺癌卡培他滨耐药细胞株PANC-1/CAP 细胞增殖、凋亡和卡培他滨耐药性的影响,双荧光素酶报告基因验证miR-429 与PTEN 的靶向关系,Western blotting 实验进一步检测miR-429 对PTEN-PI3K/AKT信号通路的调控作用。结果：miR-429 在胰腺癌PANC-1 细胞和PANC-1/CAP细胞中的表达水平高于人胰腺导管上皮细胞（HPDE6-C7）（P<0.05 或P<0.01）,敲降miR-429 可显著抑制PANC-1/CAP细胞增殖活力、促进细胞凋亡及下调细胞卡培他滨耐药性,且双荧光素酶报告基因证实miR-429 靶向作用PTEN并下调其表达水平（P<0.05 或P<0.01）;敲降miR-429 可通过靶向上调PTEN并阻断PI3K/AKT信号通路进而显著抑制PANC-1/CAP细胞增殖活力,从而下调PANC-1/CAP细胞对卡培他滨的耐药性（P<0.05 或P<0.01）。结论：miR-429/PTEN-PI3K、AKT信号通路与胰腺癌卡培他滨耐药性存在调控关系,且敲降miR-429 可逆转PANC-1/CAP对卡培他滨的耐药性。     

PI3K/AKT/MTOR信号通路对肾癌A498细胞增殖、迁移及侵袭的影响研究

目的 探讨PI3K/AKT/MTOR信号通路对肾癌A498细胞增殖、迁移及侵袭的影响.方法 选用PI3K/MTOR双重阻断剂NVP-BEZ235体外处理肾癌A498细胞,浓度分别为0、100、250、500 nmol/L.48 h后采用蛋白质印迹法(Western blot)检测肾癌A498细胞中AKT和MTOR蛋白磷酸化情况;MTT法检测细胞增殖情况;细胞划痕实验检测细胞迁移能力;Transwell小室检测细胞侵袭能力;Western blot法检测细胞中E-Cadherin和PTEN蛋白表达变化.结果 肾癌A498细胞中p-AKT、MTOR、p-MTOR、E-Cadherin、PTEN的表达及细胞增殖率、迁移率、穿膜细胞数量各自在不同NVP-BEZ235浓度下比较,差异均有统计学意义(P﹤0.01).与0 nmol/L组比较,100、250、500 nmol/L的NVP-BEZ235处理肾癌A498细胞后,细胞中磷酸化蛋白p-AKT和p-MTOR的表达均下调,细胞增殖率下降,细胞迁移率下降,穿膜细胞数量减少,细胞中E-Cadherin和PTEN蛋白表达均上调,差异均有统计学意义(P﹤0.05).结论 通过阻断PI3K/AKT/MTOR信号通路可以抑制肾癌A498细胞的增殖、迁移和侵袭,可能与上调细胞中E-Cadherin和PTEN蛋白表达有关.     

MicroRNA-106b promotes pituitary tumor cell proliferation and invasion through PI3K/AKT signaling pathway by targeting PTEN

The purpose of this study was to investigate the expression of microRNA-106b (miR-106b) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in pituitary tumor and to confirm whether miR-106b promotes proliferation and invasion of pituitary tumor cells through the PI3K/AKT signaling pathway by targeted regulation of PTEN expression, and thereby to find new targets for the treatment of pituitary tumor. Fifty-five cases of pituitary tumor tissue samples were collected, including 29 cases of invasive pituitary tumor, non-invasive 26 cases, and 8 normal pituitaries. The expression level of miR-106b in pituitary tumor tissue was detected by quantitative real-time PCR, and the expression of PTEN protein was detected by immunohistochemistry. PTEN 3′-untranslated region (UTR) luciferase vector was constructed, and dual-luciferase reporter gene assay was employed to examine the effect of miR-106b on PTEN 3′-UTR luciferase activity. AtT-20 cells were transfected with miR-106b mimics, miR-106b inhibitor, PTEN expression plasmid, and miR-106b mimics + PTEN expression plasmid respectively, and the changes in cellular proliferation and invasion were observed via MTT method and transwell assay respectively. PTEN messenger RNA (mRNA) expression was determined by quantitative real-time PCR, and western blotting was performed to detect the expression of PTEN, PI3K, AKT, and pAKT. miR-106b showed up-regulation in invasive pituitary tumor tissue: the expression level was significantly up-regulated compared with normal tissues and the non-invasive pituitary tumor tissue (P < 0.05). The positive rate of PTEN protein expression in invasive pituitary tumor tissues was significantly lower than in normal and non-invasive tissues (P < 0.01). Dual-luciferase reporter gene assay showed that miR-106b could bind to the 3ʹ-UTR of PTEN specifically and significantly inhibited the luciferase activity, cutting the 46 % (P < 0.01). Down-regulation of miR-106b or up-regulation of PTEN could suppress cell proliferation and invasion of AtT-20 cells, and PTEN expression plasmid could partially simulate the function of miR-106b. Expression of PTEN mRNA and protein decreased significantly in AtT-20 cells overexpressing miR-106b. The expression levels of PI3K and p-AKT were significantly inhibited by miR-106b inhibitor and increased by miR-106b mimics. The expression of miR-106b showed up-regulation in pituitary tumor tissues, while the protein expression of PTEN presented opposite results. The findings of this study further demonstrated that miR-106b as an oncogene regulated the pituitary tumor cell proliferation and invasion in vitro by directly targeting PTEN through the PI3K/AKT signaling pathway. Our study suggests that miR-106b and PTEN are likely to serve as potential diagnostic biomarkers or therapeutic targets for pituitary tumor treatment in the future.

     

食管鳞癌细胞外泌体中miR-130a对血管新生的作用及其机制

目的 探讨食管鳞癌细胞外泌体中的miR-130a对血管新生的作用及其机制.方法 提取食管上皮细胞HEEC、食管鳞癌细胞TE-13和Eca-109所分泌的外泌体及转染miR-130a mimic、miR-130a inhibitor及其阴性对照(NC)后的Eca-109细胞外泌体,并与人脐静脉血管内皮细胞HUVEC共孵育...     

RFC5, regulated by circ_0038985/miR-3614-5p,functions as an oncogene in the progression of colorectal cancer

Replication factor C 5 (RFC5) is involved in a variety of biological functions of cancer. However, the expression pattern of RFC5 and the underlying mechanisms in colorectal cancer (CRC) remain elusive. Here, we show that RFC5 is significantly upregulated in CRC tissues and cells. Patients with CRC and increased RFC5 levels have an unfavorable prognosis. RFC5 can promote the proliferation, migration, and invasion of CRC cells and inhibit the apoptosis of CRC cells. Additionally, upstream of RFC5, we constructed the competing endogenous RNA network and confirmed that RFC5 in this network was inhibited by miR-3614-5p by directly targeting its 3′-untranslated regions. We verified that circ_0038985, which is positively correlated with RFC5, directly targeted miR-3614-5p. Overexpression of circ_0038985 promoted CRC cell migration and invasion, and these effects were partially reversed by the reintroduction of miR-3614-5p. Moreover, we found that RFC5 may promote the vascular endothelial growth factor A (VEGFa)/vascular endothelial growth factor receptor 2 (VEGFR2)/extracellular signal-regulated protein kinase (ERK) pathway. The knockdown of RFC5 reduced CRC tumorigenesis in vivo. Collectively, these data demonstrate that the circ_0038985/miR-3614-5p/RFC5 axis plays a critical role in the progression of CRC, and RFC5 may promote CRC progression by affecting the VEGFa/VEGFR2/ERK pathway.     

miR-19通过靶向PTEN调节PI3K-Akt通路促进子宫内膜癌KLE细胞 的侵袭和迁移

目的：分析miR-19对PTEN及PI3K-Akt通路的调节作用,揭示miR-19和PTEN对子宫内膜癌KLE细胞侵袭、迁移的影响及其机制。方法：收集2017年5月至2020年8月河北医科大学第一医院收治的74例子宫内膜癌患者经手术切除（术前未接受放化疗等治疗）且病理确诊为子宫内膜癌的肿瘤组织及对应癌旁组织,采用qPCR和WB法检测PTEN在子宫内膜癌组织中的表达水平以及转染miR-19模拟物或抑制物对KLE细胞中PTEN表达的影响。通过TargetScan及双荧光素酶报告基因实验预测并验证PTEN是否为miR-19的靶基因,将KLE细胞随机分为对照（NC）组、miR-19模拟物组和miR-19+PTEN组,分别转染阴性对照片段（miR-NC）、miR-19 模拟物或共转染 miR-19 模拟物+PTEN 过表达载体,采用 Transwell 和细胞划痕实验检测 miR-19 和PTEN对KLE细胞迁移和侵袭能力的影响,WB法检测对PI3K-Akt通路相关蛋白表达的影响。结果：子宫内膜癌组织中PTEN的mRNA和蛋白表达水平均明显低于癌旁组织（均P<0.01）。miR-19能与PTEN mRNA的3’-UTR特异性结合,上调miR-19的表达能抑制PTEN的mRNA和蛋白的表达,下调miR-19的表达则出现相反的结果（均P<0.01）。与miR-NC组相比,miR-19 模拟物组的迁移、侵袭细胞数以及划痕愈合率均显著升高（均 P<0.01）,而 miR-19+PTEN 组的细胞迁移和侵袭能力以及划痕愈合率较miR-19摸拟物组则明显降低（均P<0.01）;与miR-NC 组相比,miR-19 模拟物组中 PTEN 蛋白的表达明显降低,而p-Akt 308和p-Akt 473蛋白的表达明显升高,Akt蛋白的表达无明显变化（均P<0.01）;而在miR-19+PTEN组中,p-Akt 308和p-Akt 473蛋白的表达均明显低于miR-19模拟物组（均P<0.01）。结论：miR-19可能通过抑制PTEN的表达从而活化PI3K-Akt通路,进而促进子宫内膜癌KLE细胞的迁移和侵袭。     

miR-145靶向KLF5抑制膀胱癌BIU-87细胞增殖、侵袭、迁移的机制研究

目的 研究miR-145靶向调控锌指蛋白转录因子5(KLF5)抑制膀胱癌BIU-87细胞增殖、侵袭、迁移的机制.方法 miR-145 mimics对BIU-87细胞进行转染,实验分为对照组、miR-145阴性对照组、miR-145 mimics组,SV-HUC-1细胞作为SV-HUC-1组.实时荧光定量法(RT-qPC...     

miR-19b对卵巢癌细胞侵袭和迁移的作用探讨

目的:探讨微小RNA-19b（microRNA-19b,miR-19b）在卵巢癌细胞侵袭和迁移中的作用机制。方法:应用qRT-PCR方法检测正常卵巢组织、卵巢癌组织及卵巢癌细胞系(SKOV-3、OVCAR-3)中miR-19b的表达情况。将miR-19b抑制剂或阴性对照寡核苷酸转染到OVCAR-3细胞中,Transwell实验检测miR-19b的表达对卵巢癌细胞侵袭和迁移能力的影响。免疫印迹分析（Western blot）技术检测miR-19b对第10号染色体缺失的磷酸酶和张力蛋白基因（phosphatase and tensin homolog deleted on chromosome ten,PTEN）的表达及对PTEN/AKT信号通路相关蛋白表达水平的影响。双报告基因实验用于检测miR-19b与PTEN的 3’-UTR区之间的相互作用。结果:与正常卵巢组织比较,卵巢癌组织及卵巢癌细胞系 SKOV-3和OVCAR-3中miR-19b高表达,其相对表达水平分别为3.56±0.68、3.01±0.02、3.78±0.04（P均<0.05）。Transwell 实验表明,抑制miR-19b 的表达可降低OVCAR-3细胞的侵袭和迁移能力。上调miR-19b的表达可抑制OVCAR-3细胞中PTEN蛋白的表达水平,并使磷酸化的AKT蛋白的表达水平显著升高。双报告基因检测结果显示,与对照组相比,miR-19b可与PTEN的3’-UTR区结合使其重组载体的荧光素酶活性下降。结论:miR-19b在卵巢癌细胞中存在异常高表达,可促进卵巢癌细胞的侵袭和迁移能力,有望作为卵巢癌患者潜在的生物标志物和治疗靶点。     

Lamin A/C protein is overexpressed in tissue-invading prostate cancer and promotes prostate cancer cell growth, migration and invasion through the PI3K/AKT/PTEN pathway

Prostate cancer (PC) remains the second most common cause of cancer-related death in Western countries. A previous proteomics study suggested that the nuclear membrane protein lamin A/C to be a maker to discriminate low- and high-Gleason score tumors and to identify high-risk cancers. To characterize its function in PC cells, we performed a detailed expression analysis in PC tissue and explored the consequences of down or upregulation of lamin A/C in PC cells. Our results confirm an increased lamin A/C protein expression in high-risk cancers and show association of expression with tumor cell formations at the invasion fronts of tumors and in invasion 'spearheading' tumor cell clusters. In the prostate tumor cell lines, LNCaP, DU145, and PC3 small hairpin RNA knockdown or overexpression of lamin A/C resulted in inhibition or stimulation, respectively, of cell growth, colony formation, migration and invasion. Further mechanism studies suggested that the lamin A/C-related malignant behavior is regulated through modulation of the phosphoinositide 3-kinase (PI3K)/AKT/PTEN signaling pathway. Western blot results indicated that knockdown or overexpression of lamin A/C decreased or increased, respectively, protein levels of the PI3K subunits p110 and p85 in all three cell lines; phosphor-AKT in the PTEN-negative cell lines LNCaP and PC3, and, increased or decreased, respectively, PTEN protein levels in PTEN-positive DU145 cells. Together, our data suggest that lamin A/C proteins are positively involved in malignant behavior of PC cells through the PI3K/AKT/PTEN pathway. Lamin A/C may represent a new oncogenic factor and a novel therapeutic target for PC.     

MiR-150-5p Suppresses Colorectal Cancer Cell Migration and Invasion through Targeting MUC4

Growing evidence suggests that miR-150-5p has an important role in regulating genesis of various types of cancer. However, the roles and the underlying mechanisms of miR-150-5p in development of colorectal cancer (CRC) remain largely unknown. Transwell chambers were used to analyze effects on cell migration and invasion by miR-150-5p. Quantitative real-time PCR (qRT-PCR), Western blotting and dual-luciferase 3’ UTR reporter assay were carried out to identify the target genes of miR-150-5p. In our research, miR-150-5p suppressed CRC cell migration and invasion, and MUC4 was identified as a direct target gene. Its effects were partly blocked by re-expression of MUC4. In conclusiomn, miR-150-5p may suppress CRC metastasis through directly targeting MUC4, highlighting its potential as a novel agent for the treatment of CRC metastasis.     

miR-145-5p靶向TAGLN2调控结直肠癌SW620细胞侵袭和迁移的机制探讨

目的:探究微小RNA-145-5p（miR-145-5p）在结直肠癌组织和细胞中的表达情况及其靶向调控肌动蛋白凝胶蛋白2（TAGLN2）对结直肠癌细胞侵袭和迁移能力的影响。方法:采用实时荧光定量PCR（qPCR）技术对48例结直肠癌患者癌组织、配对癌旁组织、结直肠癌细胞株（HCT8、SW620、HCT116、HT-29）及结直肠黏膜细胞FHC中的miR-145-5p和TAGLN2 mRNA表达进行定量分析。将SW620细胞设为空白对照组、miR-145-5p mimics组、mimics-NC组、pcDNA3.1-TAGLN2组、pcDNA3.1-Vector组和miR-145-5p mimics+pcDNA3.1-TAGLN2组,采用qPCR检测miR-145-5p和TAGLN2 mRNA表达,采用Transwell法检测细胞侵袭及迁移能力,采用免疫印迹法（Western blot）检测TAGLN2蛋白及EMT相关蛋白表达,采用双荧光素酶报告实验检测miR-145-5p和TAGLN2间的靶向关系。结果:miR-145-5p在结直肠癌组织中的表达水平显著低于癌旁组织（P<0.05）,并与结直肠癌患者的TNM分期和淋巴结转移相关（均P<0.05）;TAGLN2在结直肠癌组织中的表达水平显著高于癌旁组织,并与miR-145-5p表达呈负相关（P<0.05）;miR-145-5p和TAGLN2在结直肠癌HCT8、SW620、HCT116和HT-29细胞中的表达水平显著低于或高于FHC细胞（均P<0.05）。miR-145-5p过表达可降低SW620细胞的侵袭和迁移能力。miR-145-5p靶向调控TAGLN2表达,单独转染TAGLN2阳性质粒可增加SW620细胞的侵袭和迁移能力,与miR-145-5p mimics同时转染后,TAGLN2蛋白、波形蛋白（Vimentin）和神经钙黏素（N-cadherin）表达降低,上皮钙黏素（E-cadherin）表达升高,TAGLN2对SW620细胞侵袭和迁移能力的增强作用被显著抑制。结论:miR-145-5p在结直肠癌中呈低表达状态,其表达水平与结直肠癌患者的TNM分期和淋巴结转移密切相关,miR-145-5p靶向调控TAGLN2抑制结直肠癌细胞的侵袭和迁移能力。