Non-coding RNA and lung cancer progression

非编码RNA与肺癌进展

阅读:1

Abstract

Lung cancer (LC) is a major killer disease globally. This situation is further supported by yearly increase in new LC cases and its poor 5-year survival which is less than 15%. Although a large percentage of LC cases have been attributed to smoking, a considerable amount of nonsmokers also develops this disease, thereby suggesting a genetic and/or epigenetic undertone to LC development. Several growth-related genes such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) as well as tumor suppressor genes such as p53 have been implicated in LC pathogenesis and progression. Likewise, the genome only contains approximately 1% of coding regions. Hence, noncoding portion of the genome such as noncoding RNAs (ncRNAs) has been studied and discovered to play a cogent role in LC pathogenesis. More precisely, microRNAs (miRNAs) and long ncRNAs (lncRNAs) have been studied for decades. Posttranscriptional gene modulation function of miRNAs is well established and characterized. Likewise, the antagonizing interaction between lncRNAs and miRNAs had also been proven to further control gene expression during healthy and disease conditions like LC. More recently, renewed attention toward circular RNAs [circular RNAs (circRNAs)] study showed that circRNAs can also sponge miRNAs to modulate gene expressions too. Hence, miRNAs, lncRNAs, and circRNAs seem to function within a circuit to optimally determine which gene is needed to be upregulated or downregulated in biological system. Therefore, this review will discuss important ncRNAs, namely miRNA, lncRNA, and circRNA in LC progression. Paracrine effect of exosomal ncRNA will be also reviewed. In addition, the prospect of these ncRNAs in enhancing better LC treatment will be highlighted as well.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。