医学
心肌梗塞
血管生成
细胞凋亡
内科学
肿瘤科
作者
Soudeh Ghafouri-Fard,Tahereh Azimi,Mohammad Taheri
标识
DOI:10.1016/j.biopha.2020.111040
摘要
Myocardial Infarction Associated Transcript (MIAT) is a non-coding transcript which is located on chromosome 22q12.1. This lncRNA can regulate expression of genes at both transcriptional and post-transcriptional stages. It has been firstly recognized as a susceptibility locus for myocardial infarction. Subsequently, its role in the development of several human cancers has been acknowledged. Numerous researches have reported the impact of MIAT silencing on the reduction of cell viability, proliferation and invasion while enhancement of cellular senescence and apoptosis. Consistently, investigations in the xenograft models have verified MIAT role in the promotion of tumor growth. Numerous microRNAs such as miR-214, miR-22-3p, miR-520d-3p, miR-203a, miR-29a-3p, miR-141, miR-150, miR-302, miR-29, and miR-155-5p have functional interactions with this lncRNA. Moreover, dysregulation of MIAT has been associated with abnormal activity of numerous cancer-related signaling cascades such as Hippo, PI3K/Akt/c-Met and Wnt/β-catenin. In the current review, we explain the role of MIAT in the cancer evolution based on the outcomes of in vitro, in vivo and clinical studies.
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