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肿瘤的发生是一个多因素参与的阶段性演进过程,研究发现mi R-221/mi R-222在多数肿瘤中的表达失调,通过负调控抑癌基因或癌基因的表达,促进或抑制肿瘤的发生、发展。现就mi R-221/mi R-222在肿瘤中的表达、作用及其临床意义作一综述,并探讨mi R-221/mi R-222在肿瘤治疗中的潜在价值。 相似文献
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Maspin是一种肿瘤抑制基因,属于丝氨酸蛋白酶抑制剂超家族成员,近年研究发现其通过抑制肿瘤血管生成,增加细胞黏附性,促进肿瘤细胞的凋亡,抑制肿瘤的发生和发展,并具有肿瘤转移抑制作用,有可能为基因治疗提供一条新途径。 相似文献
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miR-17~92基因簇编码6种成熟的miRNA,包括miR-17、miR-20a、miR-18a、miR-19a、miR-19b和miR-92a-1,是一类典型的致癌多作用子miRNA。miR-19(包括miR-19a和miR-19b)是其中最重要的致癌miRNA,在淋巴瘤、白血病、肺癌、乳腺癌、多发性骨髓瘤等肿瘤中均表达上调,成为研究的热点之一。miR-19可通过抑制靶基因如PTEN、PP2A、Bim、SOCS1等促进肿瘤的增殖、侵袭和转移,与PI3K-AKT-mTOR信号转导通路关系密切,在肿瘤的发生发展中起着非常重要的作用。 相似文献
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[目的]探讨miR-221和miR-222在胃癌中的表达及与临床病理特征的关系。[方法]应用茎环RT-PCR方法检测32例胃癌及癌旁胃黏膜组织中miR-221和miR-222表达,分析miR-221和miR-222表达与胃癌临床病理指标的关系。[结果]胃癌组织miR-221和miR-222表达明显高于对应的正常胃黏膜组织(P〈0.05),且胃癌与正常胃黏膜组织中miR-221和miR-222比值也有显著性差异(P=0.05)。miR-222表达与胃癌分化程度相关(P=0.046);miR-221表达与淋巴结转移相关(P=0.013)。[结论]miR-221和miR-222在胃癌中表达明显上调是胃癌的重要标志,但两者在胃癌发生发展的不同阶段,可能发挥不同的效应。 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(miRNA)与肿瘤的发生发展密切相关。miR-139是一种具有抑癌作用的miRNA分子,在多种肿瘤组织中表达降低,而过表达 miR-139可通过多种靶基因抑制肿瘤细胞的增殖、迁移和侵袭,并诱导其凋亡。因此,miR-139在肿瘤的临床诊断、治疗及预后判断等方面具有潜在的应用前景。 相似文献
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microRNA-221和microRNA-222与恶性肿瘤的研究进展 总被引:1,自引:0,他引:1
微RNA(micmRNA)-221和microRNA-222是成簇的microRNA,在恶性肿瘤中起促癌作用,在胶质母细胞瘤、前列腺癌、乳头状甲状腺癌等恶性肿瘤中高表达.microRNA-221和microRNA-222通过调控其特定的靶基因行使促癌作用.在所有预测的靶基因中,p27kip1和p57kip2是已被验证的靶基因,microRNA-221和microRNA-222通过下调p27kip1和p57kip2的表达来促进肿瘤的形成和生长. 相似文献
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微RNA(microRNA)-221和microRNA-222是成簇的microRNA,在恶性肿瘤中起促癌作用,在胶质母细胞瘤、前列腺癌、乳头状甲状腺癌等恶性肿瘤中高表达。microRNA-221和microRNA-222通过调控其特定的靶基因行使促癌作用。在所有预测的靶基因中,p27^kip1和p57^kip2是已被验证的靶基因,microRNA-221和microRNA-222通过下调p27^kip1和p57kip2的表达来促进肿瘤的形成和生长。 相似文献
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Koelz M Lense J Wrba F Scheffler M Dienes HP Odenthal M 《International journal of oncology》2011,38(2):503-511
Gastrointestinal stromal tumors (GISTs), are characterized by mutations of the KIT or platelet-derived growth factor receptor-α gene and the constitutive expression of Kit, which is currently being studied as a potential therapeutic target. In this study, we addressed the question of whether the microRNA (miRNA) 221/222 cluster (miR-221/222), which has been shown to be dysregulated in many malignancies, is linked to GIST diagnosis and prognosis, and whether it could provide a basis for possible therapeutic approaches. We analyzed the expression of miR-221 and miR-222 in 54 formalin-fixed and paraffin-embedded GISTs and corresponding peripheral non-tumorous tissue by real-time PCR. The miRNA-expression levels were studied in relation to histomorphological parameters, KIT mutation status and immunohistochemical Kit expression. miR-221 and miR-222, were reduced in most of the GISTs, in contrast to other tumors. No correlation was observed between miR-221/222 expression levels and histomorphological parameters, tumor risk grade, or KIT mutation status. However, we found major differences in miRNA expression among the different groups of immunohistochemical Kit expression, especially between Kit-negative and -positive tumors. The expression levels of miR-221 and miR-222 were significantly repressed in Kit-positive GISTs, compared to normal tissue, whereas Kit-negative GISTs exhibited a completely inverse expression pattern. This study shows for the first time that miR-221 and miR-222 can act as regulators of Kit expression in GISTs and hence reveals a new aspect in the molecular pathogenesis of these tumors. Although miR-221/222 expression does not have an impact on diagnostics, it could be considered as a tool for future therapeutic strategies for GISTs, especially for tumors with secondary resistance to tyrosine kinase inhibitors. 相似文献
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