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敲低MiR-15a表达可促进非小细胞肺癌(NSCLC)细胞在体外的发生发展并诱导其上皮-间质转化(EMT)。

Knocking down MiR-15a expression promotes the occurrence and development and induces the EMT of NSCLC cells in vitro.

作者信息

He Jia

机构信息

Department of Thoracic Surgery, Peking Union Medical College Hospital, Shuaifuyuan No. 1, Dongcheng, China.

出版信息

Saudi J Biol Sci. 2017 Dec;24(8):1859-1865. doi: 10.1016/j.sjbs.2017.11.028. Epub 2017 Nov 11.

Abstract

Non-small cell lung cancer (NSCLC) is a major type of lung cancer, with the highest mortality rate in all cancers. For all stages of NSCLC, the five-year survival is less than fifteen percent. Epithelial-mesenchymal transition (EMT) is a significant process in tumor occurrence and development, in which microRNAs may play an important role. In many cancers, microRNA-15's family member can act as suppressors or oncogenes of tumors; however, the relation between these microRNAs and EMT in lung cancer remains unclear. According to our study, miR-15a expression decreased in tumor tissues compared with than that in adjacent tissue samples. Knocking down miR-15a expression in NSCLC cells inhibited apoptosis and facilitated cell proliferation and invasion, and. Moreover, down-regulating miR-15a decreased the expression of an EMT-associated protein, E-cadherin, while increased those of vimentin, N-cadherin, and slug.

摘要

非小细胞肺癌(NSCLC)是肺癌的主要类型,在所有癌症中死亡率最高。对于所有阶段的非小细胞肺癌,五年生存率低于15%。上皮-间质转化(EMT)是肿瘤发生和发展中的一个重要过程,其中微小RNA可能起重要作用。在许多癌症中,微小RNA-15家族成员可作为肿瘤的抑制因子或癌基因;然而,这些微小RNA与肺癌中EMT的关系仍不清楚。根据我们的研究,与相邻组织样本相比,肿瘤组织中miR-15a表达降低。敲低NSCLC细胞中miR-15a的表达可抑制细胞凋亡并促进细胞增殖和侵袭。此外,下调miR-15a可降低EMT相关蛋白E-钙黏蛋白的表达,同时增加波形蛋白、N-钙黏蛋白和蜗牛蛋白的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d4e/5851900/8ba0fcf575a0/gr1.jpg

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