期刊文献+

let-7在肺癌中的研究进展 被引量:8

Research advance of let-7 in lung cancer
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摘要 目的总结let-7在肺癌发生发展中的研究现状,探讨let-7在肺癌诊断、治疗及预后方面发挥的作用。方法应用PubMed及CNKI期刊全文数据库检索系统,以"micro RNA、let-7和肺癌"为关键词,检索2008-01-01-2014-05-31相关文献,共检索到英文文献269篇,中文文献83篇。纳入标准:1)let-7在肺癌发生发展中的作用机制;2)let-7表达对肺癌诊断的关系;3)let-7在肺癌治疗中的潜在价值;4)let-7的表达对肺癌预后的意义。排除标准:1)综述类文献;2)重复及陈旧实验的文献;3)实验研究资料缺失或不全。符合分析的文献39篇。结果 let-7通过抑制相关癌基因的表达及肿瘤血管生成,抑制肺癌的发生、发展、侵袭和转移。let-7在多数肺癌组织中呈低表达,恢复let-7在肺癌组织中的表达,可以抑制肿瘤发展,提高肺癌患者对放疗及靶向治疗的敏感性。组织中let-7低表达的肺癌患者,往往提示预后不良。结论 let-7是肺癌组织中的重要标志,将对肺癌患者的诊断、治疗产生积极的影响。 OBJECTIVE To summarize the advance of let-7 in lung cancer and to investigate the significant role of let-7 in diagnosis and therapy of lung cancer. METHODS The interrelated papers were searched in pubmed and CNKI da tabase from January 1st 2008 to May 31st 2014,39 papers were analyzed according to the including standards: 1)The mechanism of let-7 in occurrence and development of lung cancer 2) Relations with diagnosis of lung cancers 3) Potential application treatment of lung cancer 4) The significance of le-7 in the prognosis of lung cancer. Excluding criteria:l) Re view articles^2) Duplicate and obsolete experimental literatures3) Experimental data missing or incomplete. According to the inclusion and exclusion criteria,33 English literatures and 6 Chinese literatures were included. RESULTS let-7 in cells can restrain the tumor angiogenesis, and participate in diverse biological functions including development, ceil prolifera- tion,differentiation,and apoptosis. Down regulation of let-7 is a common phenomenon in human lung tumors, upon resto- ring the expression of let-7 has been proved to suppress tumor growth,and to increase the radiosensitivity. CONCLUSION let-7 is a fully capable molecular marker and may yield superior diagnostic and therapeutic effects for lung cancer pa- tients.
作者 赵倩 李宝生
出处 《中华肿瘤防治杂志》 CAS 北大核心 2015年第7期564-568,共5页 Chinese Journal of Cancer Prevention and Treatment
基金 国家自然基金(81272501)
关键词 MICRO RNA LET-7 肺癌 综述文献 micro RNA let-7 lung cancer lizerature review
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参考文献39

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共引文献13

同被引文献59

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