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Updated: Nov 23, 2025

Delivery of Modified mRNA in a Myocardial Infarction Mouse Model
Published on: June 11, 2020
Myocardial Infarction Associated Transcript (MIAT): Review of its impact in the tumorigenesis
Soudeh Ghafouri-Fard1, Tahereh Azimi2, Mohammad Taheri3
1Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
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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