Effects of MIR143 on RAS signaling networks in solid tumors: a brief overview.

RAS is a well-known oncogene that plays important roles in cancer proliferation, cell survival, and cell invasion. RAS exists as three major isoforms, KRAS, HRAS, and NRAS. Mutations of these genes account for approximately 30% of all cancers. Among them, KRAS mutations are the most common, responsible for 85% and are followed by NRAS (12%) and HRAS (3%). Although the development of RAS inhibitors has been explored for a long time, so far, no effective inhibitor has been found. MicroRNAs (miRNAs) are a class of small non-coding RNAs that control the gene expression of pleural target genes at the post-transcriptional level. MiRNAs play critical roles in the physiological and pathological processes at work in cancers, such as cell proliferation, cell death, cell invasion, and metastasis. MicroRNA-143 (MIR143) is known to function as a tumor suppressor in a variety of cancers. One of its known mechanisms is suppression of RAS expression and its effector signaling pathways, such as PI3K/AKT and MAPK/ERK. Recently, we developed a potent chemically-modified MIR143-3p that enabled us to elucidate the details of the KRAS signaling networks at play in colon cancer cells and others. In this review, we will discuss the role of MIR143-3p in those RAS signaling networks that are related to various biological processes of cancer cells. Also, we will discuss the possibility of the use of MIR143 as a therapeutic drug for targeting RAS signaling networks. This article is protected by copyright. All rights reserved.