共查询到20条相似文献,搜索用时 31 毫秒
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Colorectal cancer (CRC) is a noticeable reason of cancer-associated deaths with a high incidence and mortality rate. Countless effort have been put into the improving clinical management of CRC patients including more effective tools and a wide variety of biomarkers for diagnostic, prognostic or predictive purposes. In recent years, dysregulated miRNAs have been emerged as highly sensitive and specific markers to manage CRC in an effective way. They can play key roles in carcinogenesis as potential oncogenes, tumor suppressors or regulators of cancer network. Therefore, miRNAs may serve as molecular tools that can be quantified and used in diagnostic and prognostic approaches. Growing evidence also suggests that forced expression of tumor suppressor miRNAs or inhibiting the oncogene ones, can be used as a novel treatment strategy. In this review, we focus on the clinical applications of miRNAs as promising biomarkers of early cancer detection, prognosis and treatment. 相似文献
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《Cell cycle (Georgetown, Tex.)》2013,12(20):3143-3148
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Reyhaneh Moradi Marjaneh Majid Khazaei Gordon A. Ferns Amir Avan Seyed Hamid Aghaee-Bakhtiari 《Journal of cellular physiology》2019,234(3):2306-2316
Colorectal cancer (CRC) is one of the most common cancers globally. Despite recent advances in therapeutic approaches, this cancer continues to have a poor prognosis, particularly when diagnosed late. 5-Fluorouracil (5-FU) has been commonly prescribed for patients with CRC, but resistance to 5-FU is one of the main reasons for failure in the treatment of this condition. Recently, microRNAs (miRNAs) have been established as a means of modifying the signaling pathways involved in initiation and progression of CRC and their role as oncogene or tumor suppressor have been investigated in various studies. Moreover, miRNAs through various mechanisms play an important role in inducing tumor resistance or sensitivity to anticancer drugs. Detecting and targeting these mechanisms may be a new therapeutic approach. This review summarizes the current knowledge about the potential roles of miRNAs in 5-FU resistance, with particular emphasis on molecular mechanism involved. 相似文献
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Pin Guo Quanmin Nie Jin Lan Jianwei Ge Yongming Qiu Qing Mao 《Biochemical and biophysical research communications》2013
The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with oncogenesis in GBM through deregulation of miRNAs via the c-Myc–miR-26a–PTEN signaling pathway. This may be of clinical relevance. 相似文献
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Rajab Mardani Mohammad Hassan Jafari Najaf Abadi Mahsa Motieian Sima Taghizadeh-Boroujeni Amir Bayat Alireza Farsinezhad Seyed Mohammad Gheibi Hayat Mahtab Motieian Hossein Pourghadamyari 《Journal of cellular physiology》2019,234(6):8465-8486
Leukemia is known as a progressive malignant disease, which destroys the blood-forming organs and results in adverse effects on the proliferation and development of leukocytes and their precursors in the blood and bone marrow. There are four main classes of leukemia including acute leukemia, chronic leukemia, myelogenous leukemia, and lymphocytic leukemia. Given that a variety of internal and external factors could be associated with the initiation and progression of different types of leukemia. One of the important factors is epigenetic regulators such as microRNAs (miRNAs) and long noncoding RNAs (ncRNA). MiRNAs are short ncRNAs which act as tumor suppressor (i.e., miR-15, miR-16, let-7, and miR-127) or oncogene (i.e., miR-155, miR-17-92, miR-21, miR-125b, miR-93, miR-143-p3, miR-196b, and miR-223) in leukemia. It has been shown that deregulation of these molecules are associated with the initiation and progression of leukemia. Hence, miRNAs could be used as potential therapeutic candidates in the treatment of patients with leukemia. Moreover, increasing evidence revealed that miRNAs could be used as diagnostic and prognostic biomarkers in monitoring patients in early stages of disease or after received chemotherapy regimen. It seems that identification and development of new miRNAs could pave to the way to the development new therapeutic platforms for patients with leukemia. Here, we summarized various miRNAs as tumor suppressor and oncogene which could be introduced as therapeutic targets in treatment of leukemia. 相似文献
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Reid JF Sokolova V Zoni E Lampis A Pizzamiglio S Bertan C Zanutto S Perrone F Camerini T Gallino G Verderio P Leo E Pilotti S Gariboldi M Pierotti MA 《Molecular cancer research : MCR》2012,10(4):504-515
Altered expression of miRNAs is associated with development and progression of various human cancers by regulating the translation of oncogenes and tumor suppressor genes. In colorectal cancer, these regulators complement the Vogelstein multistep model of pathogenesis and have the potential of becoming a novel class of tumor biomarkers and therapeutic targets. Using quantitative real-time PCR, we measured the expression of 621 mature miRNAs in 40 colorectal cancers and their paired normal tissues and identified 23 significantly deregulated miRNAs. We subsequently evaluated their association with clinical characteristics of the samples and presence of alterations in the molecular markers of colorectal cancer progression. Expression levels of miR-31 were correlated with CA19-9 and miR-18a, miR-21, and miR-31 were associated with mutations in APC gene. To investigate the downstream regulation of the differentially expressed miRNAs identified, we integrated putative mRNA target predictions with the results of a meta-analysis of seven public gene expression datasets of normal and tumor samples of colorectal cancer patients. Many of the colorectal cancer deregulated miRNAs computationally mapped to targets involved in pathways related to progression. Here one promising candidate pair (miR-1 and MET) was studied and functionally validated. We show that miR-1 can have a tumor suppressor function in colorectal cancer by directly downregulating MET oncogene both at RNA and protein level and that reexpression of miR-1 leads to MET-driven reduction of cell proliferation and motility, identifying the miR-1 downmodulation as one of the events that could enhance colorectal cancer progression. 相似文献
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Edyta Koscianska Vesselin Baev Konstantinia Skreka Katerina Oikonomaki Ventsislav Rusinov Martin Tabler Kriton Kalantidis 《BMC molecular biology》2007,8(1):79
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MicroRNAs (miRNAs) are one of the most abundant groups of regulatory genes in multicellular organisms, playing important roles in many fundamental cellular processes. More than four hundred miRNAs have been identified in humans and the deregulation of miRNA expression has been also shown in many cancers. Despite the postulated involvement of miRNAs in tumourigenesis, there are only a few examples where an oncogene or a tumour suppressor has been identified as a miRNA target. 相似文献14.
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microRNAs(miRNAs)是近年发现的一种高度保守的非编码小RNA, 它们通过抑制靶基因mRNA的翻译或将其降解, 在转录后水平调控基因的表达, 参与调控哺乳动物多个器官的发育过程和人类疾病的发生。miR-17-92基因簇是一个高度保守的基因簇, 编码miR-17-5p、miR-17-3p、miR-18a、miR-19a、miR-20a、miR-19b-1和miR-92-1等7个miRNAs。大量证据表明, miR-17-92基因簇miRNAs参与了心、肺、免疫系统的发育、血管生长及前脂肪细胞的分化等过程。此外, miR-17-92基因簇miRNAs在多种肿瘤中高表达, 能作为致癌基因诱发淋巴瘤和血管化肿瘤的发生, 但它也可以作为抑癌基因抑制乳腺癌细胞的增殖。文章对miR-17-92基因簇miRNAs在哺乳动物器官发育及肿瘤发生中的作用进行综述 相似文献
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EGFR and MET receptor tyrosine kinase-altered microRNA expression induces tumorigenesis and gefitinib resistance in lung cancers 总被引:1,自引:0,他引:1
Garofalo M Romano G Di Leva G Nuovo G Jeon YJ Ngankeu A Sun J Lovat F Alder H Condorelli G Engelman JA Ono M Rho JK Cascione L Volinia S Nephew KP Croce CM 《Nature medicine》2012,18(1):74-82
The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the precise mechanism by which MET overexpression contributes to TKI-resistant NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand their role in TKI-resistant NSCLCs, we examined changes in miRNA that are mediated by tyrosine kinase receptors. Here we report that miR-30b, miR-30c, miR-221 and miR-222 are modulated by both epidermal growth factor (EGF) and MET receptors, whereas miR-103 and miR-203 are controlled only by MET. We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C ? (PKC-?) and sarcoma viral oncogene homolog (SRC). These findings suggest that modulation of specific miRNAs may provide a therapeutic approach for the treatment of NSCLCs. 相似文献
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MicroRNAs (miRNAs) have quite recently emerged as a novel class of gene regulators. Many miRNAs exhibit altered expression levels in cancer, and we are only starting to understand the functional consequences of the loss or gain of particular miRNAs to the cancerous phenotype. miRNAs can be classified with regard to their role in cancer as the Good, the Bad and the Ugly. The "Good", those miRNAs that are innocent bystanders in the oncogenic transformation process, whose expression profile might even be used for cancer diagnosis or prognosis. The "Bad", those miRNAs that are causally linked to tumorigenesis and directly modify tumor suppressor- or oncogenic- pathways. And the "Ugly", those miRNAs whose inappropriate loss or gain destabilizes the cellular identity of a tumor, which indirectly results in enhanced phenotypic variability and progression of the tumor. Hereunder we will discuss the possible ways in which miRNAs can be relevant to cancer biology, and possible experimental strategies for elucidating the mechanisms involved. 相似文献
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MicroRNAs (miRNAs) are key regulators of gene expression that regulate important oncogenes and tumor suppressors. Many miRNAs can also act as oncogenes or tumor suppressors, and thus the altered expression of miRNAs is a hallmark of many cancer types. Dysregulated miRNAs provide a potentially powerful new tool that could be used to enable the characterization of tumor environments and identify novel and important oncogenic pathways. More recently, there has been growing interest in the field of miRNAs as biomarkers of cancer risk, diagnosis and response to therapy. Understanding the associations between miRNA expression and cancer phenotypes, and the potential of miRNA profiling in clinical applications, promises to be highly rewarding in the field of cancer research. 相似文献
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