miR-363-3p在胃癌组织中的表达及其对细胞系HGC-27增殖、迁移与侵袭功能的影响

目的探讨miR-363-3p在胃癌及癌旁样本中的表达差异,并分析其在胃癌细胞系中的功能。方法使用realtime PCR检测59例胃癌组织及对应癌旁组织中miR-363-3p的表达差异;使用miR-363-3p模拟物(miR-363-3pmimic)实现miRNA在胃癌细胞系HGC-27中的过表达,经增殖实验、划痕实验和Transwell实验,检测miR-363-3p对HGC-27细胞功能的影响。结果 miR-363-3p抑制胃癌细胞系HGC-27细胞增殖(P0.05,P0.01),抑制胃癌细胞系HGC-27细胞迁移(P0.001),miR-363-3p对抑制胃癌细胞系细胞的侵袭(P0.05)。结论 miR-363-3p在胃癌发生中可能起到抑癌作用,并有可能成为对胃癌治疗的一个新靶点。     

miR-490-3p通过抑制TGFβR1基因表达进而抑制结肠癌细胞的转移和侵袭

目的：研究miR-490-3p在结肠癌细胞(colorectal cancer cell,CRC)转移中的表现和生物功能,及其调控作用机制。方法：通过荧光定量PCR测定miR-490-3p在CRC细胞系的表达水平。细胞转染miR-490-3p以及shmiR-490-3p,观察miR-490-3p的过表达或基因沉默对结肠癌细胞的转移能力是否有影响。miR-490-3p的分子靶标由双荧光素酶报告基因分析和免疫印迹技术进行实验认定。通过划痕实验,Transwell小室基质渗透实验对细胞迁移和侵袭能力进行鉴定。结果：miR-490-3p在CRC细胞系中显著低表达(P<0.05,P<0.01,P<0.001,n>3)。过表达miR-490-3p显著降低CRC细胞株的细胞迁移和侵袭能力(P<0.01,n>3)。miR-490-3p的基因沉默显著增加CRC细胞株的细胞迁移和侵袭能力(P<0.01,n>3)。结肠癌细胞细胞系中过表达miR-490-3p显著降低TGFβR1的基因表达(P<0.001,n>3),miR-490-3p基因沉默显著上调TGFβR1的基因表达(P<0.001,n>3)。过表达miR-490-3p抑制TGFβR1的萤光素酶活性(P<0.001,n>3),miR-490-3p基因沉默促进TGFβR1的萤光素酶活性(P<0.001,n>3)。TGFβR1基因沉默减弱shmiR-490介导的细胞迁移和侵袭促进效应(P<0.01, n>3)。结论：miR-490-3p通过抑制TGFβR1的基因表达从而抑制CRC细胞的转移。     

miR-195-5p表达上调抑制肺癌细胞系A549的迁移和侵袭

目的探讨miR-195-5p对肺癌细胞系A549细胞迁移和侵袭的影响及其机制。方法实时荧光定量PCR检测肺癌组织及肺癌细胞系中miR-195-5p的表达;通过脂质体介导将miR-195-5p模拟物作用于A549细胞,用Transwell法检测细胞迁移和侵袭; Western blot检测细胞内上皮间质转化标志物及ZEB1的表达。结果相对于癌旁组织及人正常肺上皮细胞,miR-195-5p在肺癌组织及肺癌细胞系中低表达(P0. 001);过表达miR-195-5p可显著抑制A549细胞的迁移和侵袭(P0. 001),伴随E-cadherin蛋白表达的上调,N-cadherin和vimentin蛋白表达的下调(P0. 01);过表达miR-195-5p可抑制A549细胞ZEB1的表达(P0. 001)。结论 miR-195-5p可能通过下调ZEB1的表达,抑制肺癌细胞迁移和侵袭。     

过表达miR-5195-3p对结直肠癌细胞凋亡的影响

目的探讨miR-5195-3p对Runx相关转录因子3(RUNX3)的靶向调节作用及对结直肠癌细胞凋亡的影响。方法 RT-qPCR和Western blot分别检测结直肠癌组织与癌旁组织中miR-5195-3p和RUNX3蛋白的表达。将人结肠癌细胞系SW480随机分为5组:对照组(control)、miR-5195-3p mimic组、mimic control组、miR-5195-3p inhibitor组、inhibitor control组。Wetsern blot检测RUNX3的蛋白表达;流式细胞仪检测细胞凋亡。在SW480细胞中转染RUNX3过表达质粒后检测细胞凋亡。结果与癌旁组织中相比,miR-5195-3p在结直肠癌组织中的表达显著升高,RUNX3的蛋白表达明显降低(P0.05)。过表达miR-5195-3p显著下调了SW480细胞中RUNX3的表达,并降低细胞凋亡水平(P0.05);抑制miR-5195-3p明显上调RUNX3的表达,并上调细胞凋亡水平(P0.05)。此外与miR-5195-3p mimic组相比,RUNX3过表达质粒的共转染组显著降低细胞凋亡水平(P0.05)。结论 miR-5195-3p可能作为促癌基因在结直肠癌中发挥作用,其作用与靶向调节RUNX3相关。     

miR-129-5p靶向调控VCP抑制骨肉瘤细胞体外迁徙侵袭

目的 探讨miR-129-5p是否靶向调控VCP基因抑制骨肉瘤细胞迁徙侵袭.方法 构建miR-129-5p过表达及低表达的慢病毒载体,转染骨肉瘤细胞U2-OS;采用实时荧光定量PCR检测上调及下调miR-129-5p的U2-OS细胞中miR-129-5p的表达量;采用RT-PCR和Western blot技术检测VCP mRNA和蛋白表达;采用划痕实验和Transwell侵袭实验检测细胞迁徙、侵袭情况.结果 实时荧光定量PCR结果显示U2-OS细胞中miR-129-5p表达被明显上调或下调;RT-PCR和Western blot检测结果显示:miR-129-5p上调U2-OS细胞组中VCP mRNA和蛋白表达水平显著低于阴性对照细胞组(阴性慢病毒转染);miR-129-5p下调U2-OS细胞组中VCP mRNA和蛋白表达水平显著高于阴性对照细胞组;miR-129-5p上调U2-OS细胞迁徙和侵袭力显著低于阴性对照细胞,miR-129-5p下调的U2-OS细胞迁徙和侵袭力显著高于阴性对照细胞.结论 miR-129-5p靶向调控VCP的表达而抑制骨肉瘤细胞迁徙和侵袭能力.     

miR-874-3p靶向结合SDC1抑制胶质瘤血管生成拟态

目的本研究旨在探讨miR-874-3p调控胶质瘤血管生成拟态的潜在分子机制。方法应用实时定量PCR检测miR-874-3p在胶质瘤细胞系U87细胞中的表达水平;应用双荧光素酶报告基因分析系统检测miR-874-3p和SDC1的结合作用;应用CCK-8法、transwell法、体外管形成实验检测miR-874-3p或SDC1表达变化对U87细胞增殖、迁移、侵袭和管形成能力的影响。结果 miR-874-3p在U87细胞中低表达,过表达miR-874-3p显著抑制U87细胞的增殖、迁移、侵袭和管形成能力。SDC1在U87细胞中的表达上调,沉默SDC1显著抑制U87细胞增殖、迁移、侵袭和管形成能力。miR-874-3p靶向SDC1 3'UTR。结论 miR-874-3p通过靶向结合SDC1抑制胶质瘤血管生成拟态。     

lncRNA MAFG-AS1靶向miR-3180-3p调控口腔鳞癌HSC4细胞增殖和凋亡

目的：探讨长链非编码RNA(lncRNA)MAFG反义RNA1(MAFG-AS1)靶向miR-3180-3p对口腔鳞癌细胞增殖和凋亡的影响。方法：实时定量PCR检测口腔鳞癌组织和对应正常黏膜中MAFG-AS1和miR-3180-3p表达。以口腔鳞癌细胞HSC4为研究对象,分别构建干扰MAFG-AS1、过表达miR-3180-3p或抑制miR-3180-3p表达的口腔鳞癌细胞株,CCK-8、平板克隆实验、流式细胞术、蛋白印迹法检测细胞活力、克隆形成数、凋亡率及cleaved-caspase 3、cleaved-caspase 9表达。荧光素酶报告实验验证MAFG-AS1和miR-3180-3p的靶向关系。结果：与正常黏膜比较,口腔鳞癌组织MAFG-AS1表达显著升高（P<0.05）,miR-3180-3p表达显著降低（P<0.05）。干扰MAFG-AS1或过表达miR-3180-3p均可降低HSC4细胞活力和克隆形成数（P<0.05）,促进细胞凋亡（P<0.05）,上调cleaved-caspase 3和cleaved-caspase 9蛋白表达（P<0.0...     

miR-142-3p 靶向ATG4c 调控RAW264.7 巨噬细胞自噬

目的:研究miR-142-3p 对自噬相关基因ATG4c 的靶向调控作用,探究miR-142-3p 影响RAW264.7 细胞自噬途径的作用机制。方法:生物信息学软件分析miR-142-3p 的靶基因为ATG4c,构建pMIR-Report-ATG4c 和pMIR-Report-ATG4c mut 重组质粒,双荧光素酶报告系统、qRT-PCR、Western blot 验证miR-142-3p 与ATG4c 的靶向作用;将做不同处理的RAW264.7 细胞分为4 组:正常细胞作为对照、50 ng/ ml 雷帕霉素作用2 h、EBSS 饥饿作用12 h、10 nmol/ L 的3-甲基腺嘌呤(3-MA)作用12 h 后,实时荧光定量PCR(qRT-PCR)检测miR-142-3p 不同干预组中的相对表达情况;将miR-142-3p mimics、miR- 142-3p inhibitor 及miR-142-3p control 分别转染到RAW264.7 细胞中,检测miR-142-3p 和LC3域的相对表达。结果:双荧光素酶报告系统、qRT-PCR、Western blot 验证miR-142-3p 通过靶向作用于ATG4c 的3忆-UTR 抑制其表达;与对照组相比,雷帕霉素和饥饿处理的RAW264.7 细胞miR-142-3p 明显上调,而3-MA 处理组miR-142-3p 明显下调;与miR-142-3p control 组相比,转染miR-142-3p mimics 组中LC3域蛋白表达显著下调,而miR-142-3p inhibitor 组中表达显著上调。结论:miR-142-3p 通过靶向调控自噬相关基因ATG4c,参与RAW264.7 小鼠巨噬细胞自噬的调控。     

miR-155-5p在宫颈癌血清中的表达及其对宫颈癌细胞的影响

 目的：检测miR-155-5p在不同宫颈疾病患者血清中的表达差异,并分析其对宫颈癌细胞增殖、细胞周期和凋亡的影响,探讨miR-155-5p在宫颈癌发生、发展中的可能作用机制。方法：采用SYBR GreenⅠ实时荧光定量PCR法,检测并分析比较miR-155-5p在不同宫颈疾病患者血清中的表达差异。利用miR-155-5p mimic或inhibitor提高或降低宫颈癌细胞中miR-155-5p的表达。CCK-8法和流式细胞术检测宫颈癌细胞的增殖、细胞周期和凋亡。结果：宫颈癌组血清中miR-155-5p的表达高于宫颈炎组和健康对照组（P<0.05）,宫颈上皮内瘤样病变组和宫颈癌组血清中miR-155-5p的表达差异无统计学意义（P>0.05）。与空白组、脂质体组和阴性对照组相比,转染100 nmol/L和200 nmol/L miR-155-5p mimic的SiHa细胞中,S期细胞比例升高,凋亡细胞比例降低（P<005）。转染100 nmol/L和200 nmol/L miR-155-5p inhibitor的SiHa细胞中,G2/M期细胞比例明显增多（P<005）。结论：(1)宫颈癌患者血清中miR-155-5p表达较健康对照人群上调,可能作为宫颈癌早期诊断的肿瘤分子标志物。(2)miR-155-5p对宫颈癌HeLa细胞增殖、细胞周期和凋亡无明显影响。(3)miR-155-5p可促进宫颈癌SiHa细胞进入S期,并抑制SiHa细胞凋亡,提示miR-155-5p可能在宫颈鳞癌发生、发展中起作用。     

microRNA-424-5p对人胃癌细胞SGC-7901自噬的影响及机制

目的研究microRNA-424-5p(miR-424-5p)对人胃癌细胞SGC-7901自噬的影响及可能机制。方法培养人正常胃黏膜上皮细胞GES和人胃癌细胞SGC-7901,应用实时定量PCR方法检测miR-424-5p的表达水平;应用Lipofectamine LTX试剂将化学合成的miR-424-5p agomir和miR-424-5p antagomir转染人胃癌细胞SGC-7901,验证转染效率后应用MTT方法检测细胞活力;应用免疫荧光法检测自噬标记物微管相关蛋白轻链-3(LC3)和自噬降解底物p62/SQSTM1在SGC-7901细胞的分布;应用Western blot方法检测LC3-Ⅱ、p62/SQSTM1和自噬相关蛋白Beclin1的蛋白表达水平。结果 miR-424-5p在人胃癌细胞SGC-7901中呈低表达,miR-424-5p过表达显著抑制人胃癌细胞SGC-7901的细胞活力,miR-424-5p表达沉默的作用效果与之相反。miR-424-5p过表达后自噬标记物LC3在SGC-7901细胞的胞浆内呈点状分布,荧光表达显著增强,并且LC3-II的蛋白表达水平显著上调,同时伴有自噬降解底物p62/SQSTM1在细胞浆内荧光表达显著减弱,蛋白表达下调,此外,自噬相关蛋白Beclin1的蛋白表达水平显著上调;miR-424-5p表达沉默的作用效果与之相反。结论 miR-424-5p过表达明显抑制人胃癌细胞SGC-7901的细胞活力,诱导细胞发生自噬,其机制之一可能与自噬相关蛋白Beclin1上调有关。     

Inhibition of hsa_circ_0001313 (circCCDC66) induction enhances the radio-sensitivity of colon cancer cells via tumor suppressor miR-338-3p: Effects of cicr_0001313 on colon cancer radio-sensitivity

Circular RNA_0001313 (circ_0001313), also known as circCCDC66, is a novel circRNA that recently found to be upregulated in colon cancer tissues and promote colon cancer progression. However, the role of circ_0001313 in regulating radio-sensitivity of colon cancer and its molecular mechanism remain undetermined. Here we found circ_0001313 was significantly upregulated and miR-338-3p was downregulated in radio-resistant colon cancer tissues compared to radio-sensitive tissues. Radiation treatment in colon cells triggered a remarkable upregulation of circ_0001313 and a downregulation of miR-338-3p. Knockdown of circ_0001313 reduced cell viability, colony formation rate and increased caspase-3 activity in colon cancer cells under irradiation. Moreover, circ_0001313 act as a sponge for miR-338-3p in colon cancer cells. Furthermore, miR-338-3p could reverse the effects of circ_0001313 knockdown on cell viability, colony formation, and caspase-3 activity. These findings revealed that knockdown of circ_0001313 could induce radio-sensitivity of colon cancer cells by negatively regulating miR-338-3p.     

miR-338-3p inhibits the proliferation and migration of gastric cancer cells by targeting ADAM17

Background: MicroRNAs (miRNA) have been documented playing a critical role in cancer progression. Although miR-338-3p has been implicated in several cancers, its role in gastric cancer is still unknown. The aim of our study was to investigate the role of miR-338-3p in gastric cancer progression. Methods: Expression levels of miR-338-3p in gastric cancer cell lines and tissues were determined by quantitative real-time PCR (qRT-PCR). The effect of miR-338-3p on proliferation was evaluated by MTT assay, cell migration and invasion were evaluated by transwell migration and invasion assays. Furthermore, luciferase reporter assay was conducted to confirm the target gene of miR-338-3p, and the results were validated in gastric cancer cells. Results: In the present study, we found that miR-338-3p was down-regulated in both gastric cancer cell lines and tissues. Enforced expression of miR-338-3p inhibited proliferation, migration and invasion of gastric cancer cells in vitro. Moreover, we identified A disintegrin and metalloproteinase 17 (ADAM17) gene as potential target of miR-338-3p. Importantly, ADAM17 rescued the miR-338-3p mediated inhibition of cell proliferation, migration and invasion. Conclusions: Our study suggested that miR-338-3p is significantly decreased in gastric cancer, and inhibits cell proliferation, migration and invasion partially via the downregulation of ADAM17. Thus, miR-338-3p may represent a potential therapeutic target for gastric cancer intervention.     

miR-454-3p靶向BPTF表达调控肺癌细胞A549增殖、迁移和侵袭

目的探讨miR-454-3p对肺癌细胞增殖、迁移和侵袭的影响及分子机制。方法采用RT-PCR技术检测miR-454-3p在肺癌组织以及肺癌细胞株中的表达,以表达量最低的肺癌细胞A549为后续分析对象,将miR-454-3p mimic转入A549细胞,RT-PCR验证miR-454-3p的过表达效率;采用CCK-8、迁移、侵袭等实验,观察转染组与对照组肺癌细胞的增殖、迁移和侵袭情况;生物信息学预测BPTF是miR-454-3p的靶标,构建BPTF 3′UTR荧光素酶载体,通过双荧光素酶报告基因验证miR-454-3p和BPTF的靶向关系;应用Western blot法检测BPTF的表达及迁移、侵袭相关蛋白的变化。结果RT-PCR实验表明miR-454-3p在肺癌组织和细胞中表达下调,且在A549细胞中表达最低(P<0.05)。与对照组相比,过表达miR-454-3p的肺癌细胞A549增殖能力明显降低,迁移和侵袭能力均受到抑制(P<0.05)。生物信息学软件分析BPTF为miR-454-3p的潜在靶基因,过表达miR-454-3p后BPTF的表达水平明显受到抑制。同时,迁移相关蛋白MMP-2和MMP-9表达明显下调,E-cadhern表达明显上调,而E-cadherin的负性调控N-cadherin表达下降。结论miR-454-3p可能通过靶向下调BPTF的表达,抑制肺癌细胞的增殖、迁移和侵袭能力,为肺癌的靶向治疗提供潜在靶标。     

MicroRNA-338-3p inhibits cell proliferation in hepatocellular carcinoma by target forkhead box P4 (FOXP4)

MicroRNAs (miRNAs) are a class of small, non-coding RNAs, which have demonstrated to important gene regulators, and have critical roles in diverse biological processes including cancer cell proliferation. Previous studies suggested microRNA-338-3p (miR-338-3p) was down-regulated and play tumor suppressor roles in gastric cancer, colorectal carcinoma and lung cancer. However, the role of miR-338-3p in hepatocellular carcinoma (HCC) is still unclear. In this study, we analyzed the expression of miR-338-3p in HCC tissues and HCC cell lines. We find that miR-338-3p was downregulated in HCC tissues and cell lines. Then functional studies demonstrate ectopic miR-338-3p expression significantly suppressed the in vitro proliferation and colony formation of HCC cells and cause to cell cycle arrest. Using bio-informatic method and report assay we identified a novel miR-338-3p target, FOXP4 in HCC cells. Furthermore, knockdown of FOXP4 have the similar effects in HCC corrected with miR-338-3p. These findings suggest that miR-338-3p regulates survival of HCC cells partially through the downregulation of FOXP4. Therefore, targeting with the miR-338-3p/FOXP4 axis might serve as a novel therapeutic application to treat HCC patients.     

miR-506-3p通过靶向MTDH增加前列腺癌细胞的化学敏感性

目的研究miR-506-3p对前列腺癌细胞化学敏感性的影响及其作用机制。方法用RT-qPCR检测miR-506-3p和MTDH在前列腺癌细胞系和正常前列腺细胞系中的表达水平;以紫杉醇为诱导药物构建人前列腺癌耐药细胞株PC-3/PTX,将PC-3/PTX细胞随机分为5组对照组、NC mimic组、miR-506-3p mimic组、LV-MTDH组、mimic+MTDH组,利用Lipofectamine 3000转染试剂盒分别转染对应质粒。检测其存活率、IC50值、克隆细胞数目、凋亡率以及凋亡相关蛋白的表达水平;构建MTDH野生型(WT)和突变型(MUT),用双荧光素酶报告基因实验验证miR-506-3p与MTDH之间的靶向关系;Western blot检测miR-506-3p mimic处理后PC-3/PTX细胞中MTDH的蛋白表达水平。结果miR-506-3p在前列腺癌细胞中低表达,而MTDH高表达;miR-506-3p在PC-3/PTX细胞中的表达量显著低于在前列腺癌细胞PC-3中的表达量;相比于对照组和NC mimic组,miR-506-3p mimic组的PC-3/PTX细胞的存活率、IC50值、克隆细胞数目及Bcl-2表达明显降低,凋亡率及Bax表达明显升高;MTDH野生型较突变型能使荧光素酶活性显著下降;miR-506-3p mimic组PC-3/PTX细胞中MTDH蛋白表达水平显著低于对照组和NC mimic组;相比于对照组,miR-506-3p mimic组中PC-3/PTX细胞克隆数目显著减少,凋亡率升高,而LV-MTDH组与之相反;相比于LV-MTDH组,mimic+MTDH组PC-3/PTX细胞中MTDH的表达量显著下降,细胞克隆数目减少,凋亡率升高。结论miR-506-3p通过靶向抑制MTDH的表达能增强人前列腺癌耐药细胞株PC-3/PTX的化学敏感性。     

miR-145-5p suppresses proliferation,metastasis and EMT of colorectal cancer by targeting CDCA3

MicroRNAs play a critical role in regulating the carcinogenesis of colorectal cancer (CRC). Even though its role is unclear in CRC, miR-145-5p has been reported to have anti-oncogene properties in several tumors. Our research examined the function of miR-145-5p in CRC and the potential underlying mechanism. From the bioinformatics and qRT-PCR analysis, miR-145-5p levels were lower in CRC samples and cell lines. LoVo and SW480 cells were treated with miR-145-5p mimics and inhibitor, respectively. Cell cycle, CCK-8 and EdU assays revealed that overexpression of miR-145-5p suppressed cell viability and G1/S phase transition. Conversely, miR-145-5p inhibitor promoted cell growth and cell cycle transition. Elevated miR-145-5p expression also suppressed the migration, invasion and EMT of CRC cells, while miR-145-5p reduction had a reverse effect. CDCA3 was identified as a downstream effector of miR-145-5p and had a negative correlation with the miR-145-5p expression in CRC. In addition, co-transfection of miR-145-5p inhibitor and si-CDCA3 showed that CDCA3 in SW480 cells could reverse the effect caused by miR-145-5p. In conclusion, our findings demonstrated that miR-145-5p could act as a tumor suppressor in CRC by targeting CDCA3, and serve as a diagnostic and therapeutic biomarker of CRC.     

HER2高表达胃癌细胞中miR-4728-3p表达及生物信息学分析

目的 探讨HER2高表达的胃癌细胞中miR-4728-3p表达状况及其调控靶基因所涉及的信号通路,旨在初步分析miR-4728-3p在胃癌中的作用机制及其与HER2的相关性.方法 首先采用Real-time PCR技术检测胃癌细胞株NCI-N87中miR-4728-3p及HER2 mRNA,然后通过miRanda、DIANA-microT、Targetscan和Targetmine软件预测miR-4728可能的靶基因,并通过DAVID数据库进行靶基因功能富集分析及信号转导通路富集分析.结果 miR-4728-3p及HER2 mRNA在胃癌细胞中均高表达,二者呈正相关(r=0.990,P=0.000).miR-4728-3p预测靶基因共有54个,靶基因功能主要富集于转录活性调节(P=0.014)、DNA结合(P=0.019)及蛋白质磷酸化氨基酸结合(P=0.036)等分子功能,RNA聚合酶Ⅱ启动子的转录调控(P=0.001)、转录调控(P=0.003)及细胞内信号级联(P=0.021)等生物学过程以及轴突部分(P=0.008)等细胞组分上;信号转导通路则主要富集于肿瘤通路(P=0.013)和卵母细胞减数分裂通路(P=0.041).结论 miR-4728-3p在HER2高表达的胃癌细胞中表达上调,二者表达呈正相关;生物信息学分析提示miR-4728-3p通过调控其靶基因参与胃癌的发生发展.     

miR-197-3p调控DMBT1抑制甲状腺癌细胞系增殖、迁移和侵袭

目的探讨miR-197-3p是否通过靶向调控恶性脑瘤缺失1基因(DMBT1)影响甲状腺癌细胞增殖、迁移和侵袭。方法RT-qPCR检测健康人甲状腺细胞Nthy-ori 3-1和甲状腺癌细胞SW579、CGTHW-1中miR-197-3p表达;MTT法检测SW579细胞增殖;Transwell小室法检测SW579细胞迁移和侵袭;双荧光素酶报告基因实验验证miR-197-3p是否靶向DMBT1;Western blot检测细胞DMBT1、cyclinD1、p21、MMP-2和E-cadherin蛋白表达。结果与Nthy-ori 3-1细胞比较,SW579和CGTHW-1细胞中miR-197-3p相对表达量升高(P<0.05);抑制miR-197-3p表达后,SW579细胞的增殖、迁移和侵袭能力明显受到抑制,细胞中cyclinD1蛋白和MMP-2蛋白表达降低而p21蛋白和E-cadherin蛋白表达升高;SW579细胞中miR-197-3p靶向负调控DMBT1的表达;过表达DMBT1明显抑制SW579细胞增殖、迁移和侵袭,而抑制DMBT1则能逆转miR-197-3p对SW579细胞增殖、迁移和侵袭的影响。结论miR-197-3p通过靶向调控DMBT1的表达,抑制甲状腺癌细胞增殖、迁移和侵袭。