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目的 探讨miR-375/SHOX2轴对食管鳞癌细胞侵袭迁移能力的影响,为食管鳞癌的靶向治疗寻找潜在新靶点。方法 选取对数生长期的人食管鳞癌细胞(kyse-70、kyse-30),分别过表达以及干扰miR-375和SHOX2基因,采用克隆形成、MTT、划痕、Transwell等体外细胞功能学实验检测miR-375、SHOX2对食管鳞癌细胞增殖、迁移和侵袭能力的影响,通过拯救实验验证miR-375对SHOX2的靶向调控作用。结果 与对照组的kyse-70、kyse-30细胞相比,过表达miR-375或干扰SHOX2基因后的细胞增殖率、克隆形成率和Transwell细胞穿透数均降低,差异均有统计学意义(P<0.01);与对照组的kyse-70、kyse-30细胞相比,干扰miR-375或过表达SHOX2后的细胞增殖率、克隆形成率和Transwell细胞穿透数均升高,差异均有统计学意义(P<0.01);miR-375过表达后的食管鳞癌细胞SHOX2基因表达减少,而抑制miR-375后SHOX2基因表达增强。拯救实验结果显示,共转染miR-375和SHOX2后细胞增殖和侵袭能力较对照组又有所增强。结论 miR-375抑制食管鳞癌细胞增殖和侵袭;SHOX2促进食管鳞癌细胞增殖和侵袭。miR-375靶向负调控SHOX2表达,对食管鳞癌细胞的增殖和侵袭起调控作用。 相似文献
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微小RNA miR-155在多种人体肿瘤中异常表达,与肿瘤的发生、发展及预后密切相关,被认为是癌性微小RNA(oncomiR).研究发现miR-155可通过抑制其靶基因如SHIP1、C/EBPβ、SOCS1、TP53INP1等促进肿瘤的增殖、侵袭及转移.检测miR-155的表达可对早期诊断恶性肿瘤提供重要依据,抑制其表达将成为肿瘤治疗的新方向. 相似文献
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微小RNA (miR)-203具有细胞干性抑制潜能,可通过抑制细胞干性相关转录因子的表达来调节细胞上皮样分化.研究表明miR-203在多种肿瘤组织中表达异常,包括膀胱癌、乳腺癌、结肠癌和胰腺癌等.miR-203通过调节细胞增殖、分化和凋亡在肿瘤的发生发展中发挥重要作用. 相似文献
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目的:对比分析非小细胞肺癌患者肿瘤组织、瘤旁组织和外周血清中miR-486的表达情况,探讨miR-486是否有可能成为新的非小细胞肺癌标记物。方法:选取20例临床上确诊并进行外科治疗的非小细胞肺癌病例,每个病例取3块肿瘤组织,3块正常肺组织以及3×10ml外周血液样本。另选取20例健康志愿者抽取3×10ml外周血液作为对照。提取总RNA进行qRT-PCR实验。分析外周血清和肿瘤组织中miR-486的表达情况。结果:miR-486在非小细胞肺癌肿瘤组织中呈低表达状态(P<0.05),其在瘤组织内的表达与外周血清中的表达呈正相关性(P<0.05)。结论:miR-486在人体外周血清中的表达与非小细胞肺癌存在正相关性,提示外周血清中miR-486可以成为非小细胞肺癌的预警因子。 相似文献
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miR-21对骨肉瘤细胞增殖的影响 总被引:1,自引:0,他引:1
背景与目的:微小RNA(microRNA,miRNA)是一类内源性的非编码小分子RNA,其主要通过与靶mRNA作用抑制转录后的翻译.miR-21是唯一一个在9种人类肿瘤细胞中高表达的小RNA分子.本研究旨在观察anti-miR-21反义寡核苷酸(ASO)对骨肉瘤MG-63细胞增殖的影响.方法:通过转染miR-21 ASO和对照组ASO,采用实时荧光定量RT-PCR检测MG-63细胞中miR-21的表达变化,并运用多种细胞增殖检测方法观察miR-21 ASO对MG-63细胞调控产生的系列效应.结果:与对照相比,miR-21 ASO显著减少miR-21的表达(P=0.003);克隆形成实验结果显示miR-21 ASO导致克隆形成率较对照组低(P=0.012);MTT实验结果显示转染miR-21 ASO后,MG-63细胞存活数明显低于对照组(P=0.023);在体实验结果发现miR-21 ASO抑制肿瘤细胞增殖,导致肿瘤质量较对照轻(P=0.013),形成的体积较对照小(P=0.028);流式细胞仪检测显示转染mi R-21 ASO后,MG-63细胞凋亡明显增加(P=0.022).结论:miR-21 ASO对骨肉瘤细胞miR-21水平降低有靶向特异性,转染miR-21 ASO可有效抑制miR-21的促癌作用,利用反义核酸技术可为骨肉瘤的基因治疗开辟新的径路. 相似文献
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背景与目的:研究表明miR-125a通过下调Her-2或者Her-3的表达抑制乳腺癌细胞生长,可能是指导乳腺癌治疗的靶点.本研究旨在观察miR-125a是否具有增强多西他赛对乳腺癌细胞株和裸鼠荷瘤模型的生长抑制作用.方法:转染miR-125a联合不同浓度多西他赛处理MCF-7和MDA-MB-231乳腺癌细胞株和MDA-MB-231乳腺癌裸鼠模型,观察细胞株和裸鼠接种肿瘤的生长情况.结果:miR-125a与多西他赛可协同抑制MDA-MB-231及MCF-7乳腺癌细胞株、MDA-MB-231乳腺癌裸鼠模型肿瘤的增殖,单纯转染miR-125a也可抑制MDA-MB-231及MCF-7乳腺癌细胞株的增殖.结论:miR-125a与多西他赛有协同抗乳腺癌作用,可成为乳腺癌靶向治疗的潜在靶点. 相似文献
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目的:总结国内外研究miR-145与肿瘤关系的文献,评价miR-145在肿瘤发生、发展中的作用.方法:以“miR-NAs、miR-145、肿瘤”为关键词,检索1993-2011年PubMed及CNKI期刊全文数据库.纳入标准:1)miR-145基因结构及生物学特性的研究;2)miR-145与肿瘤发生发展关系的研究;3)miR-145与肿瘤诊断、治疗和预后关系的研究.根据纳入标准,纳入分析30篇文献.结果:miR-145定位于5号染色体肿瘤相关的脆性位点上,在多种组织的恶性肿瘤中miR-145表达明显下调.过表达miR-145可抑制肿瘤细胞增殖及诱导肿瘤细胞凋亡.检测血清中miR-145的含量,有助于肿瘤的早期诊断.肿瘤组织中miR-145的表达量与患者放化疗疗效及预后密切相关.结论:miR-145是一个潜在的肿瘤生物标志,有可能成为肿瘤治疗的新靶标. 相似文献
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Wen Shi Jing Yang Siyuan Li Xiaofeng Shan Xiaosong Liu Hong Hua Chuanke Zhao Zhendong Feng Zhigang Cai Lihe Zhang Demin Zhou 《Oncotarget》2015,6(37):40172-40185
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Kinoshita T Nohata N Yoshino H Hanazawa T Kikkawa N Fujimura L Chiyomaru T Kawakami K Enokida H Nakagawa M Okamoto Y Seki N 《International journal of oncology》2012,40(1):185-193
The expression of microRNA-375 (miR-375) is significantly reduced in cancer tissues of maxillary sinus squamous cell carcinoma (MSSCC). The aim of this study was to investigate the functional significance of miR-375 and a possible regulatory role in the MSSCC networks. Restoration of miR-375 significantly inhibited cancer cell proliferation and invasion in IMC-3 cells, suggesting that miR-375 functions as a tumor suppressor in MSSCC. Genome-wide gene expression data and luciferase reporter assays indicated that lactate dehydro-genase?B (LDHB) was directly regulated by miR-375. Cancer cell proliferation and invasion were significantly inhibited by transfection of si-LDHB into IMC-3 cells, suggesting that LDHB may play a role in MSSCC oncogenic function. In clinical MSSCC specimens, LDHB mRNA levels were up-regulated in cancer tissues, which were inversely correlated with the expression of miR-375. In addition, Kaplan-Meier curves and log-rank tests revealed that the high mRNA expression levels of LDHB had a significant adverse effect on survival rate. The identification of a cancer network regulated by the miR-375 tumor suppressor could provide new insights into the molecular mechanisms of MSSCC oncogenesis. 相似文献
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Y Shen P Wang Y Li F Ye F Wang X Wan X Cheng W Lu X Xie 《British journal of cancer》2013,109(1):92-99
Background:
Chemo-resistance is one of the key causal factors in cancer death and emerging evidences suggest that microRNAs (miRNAs) have critical roles in the regulation of chemo-sensitivity in cancers. Cervical cancer is one of the most common malignancies in women and insensitive to chemotherapy clinically.Methods:
The differentially expressed miRNAs in cervical squamous cell carcinoma tissues were screened by using a microarray platform (μParaflo Sanger miRBase release 13.0). The expression of miR-375 was determined by stem-loop RT–PCR using 23 clinical cervical cancer samples and 2 cervical cancer cell lines. We exogenously upregulated miR-375 expression in SiHa and Caski cells using a pre-miRNA lentiviral vector transfection and observed its impact on paclitaxel sensitivity using MTS. The cells that stably overexpressed miR-375 were subcutaneously injected into mice to determine tumour growth and chemo-sensitivity in vivo.Results:
Twenty-one differentially expressed miRNAs were found by miRNA microarray between pro- and post-paclitaxel cervical cancer tissues. Of those, miR-375 showed consistent high expression levels across paclitaxel-treated cervical cells and tissues. Paclitaxel induced upregulated miR-375 expression in a clear dose-dependent manner. Forced overexpression of miR-375 in cervical cancer cells decreased paclitaxel sensitivity in vitro and in vivo.Conclusion:
Collectively, our results suggest that miR-375 might be a therapeutic target in paclitaxel-resistant cervical cancer. 相似文献18.
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Satoshi Yoda Kenzo SoejimaJunko Hamamoto Hiroyuki YasudaSohei Nakayama Ryosuke SatomiHideki Terai Shinnosuke IkemuraTakashi Sato Katsuhiko NaokiTomoko Betsuyaku 《Lung cancer (Amsterdam, Netherlands)》2014