Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Abstract

MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

Genetic and epigenetic drivers of neuroendocrine tumours (NET)

“…Merging the outcomes from the two groups, we found in both groups downregulation of miR-133a and upregulation of miR-183 (metastases vs primary). miR-133a has two subtypes, including miR-133a-1 and miR-133a-2, which are located on chromosomes 18q11.2, 20q13.33 (Mitchelson & Qin 2015). Low expression of miR-133a is associated with poor prognosis and promotion of tumorigenesis in several cancers (Kawakami et al 2012, Wu et al 2012, Wang et al 2014a,b, Lai et al 2015, Mirghasemi et al 2015.…”

A microRNA-mRNA expression network during oral siphon regeneration in Ciona

“…In regenerating OSs miR-9 is highly upregulated at all stages of regeneration analyzed, having no RNAseq reads and being nearly undetectable by qRT-PCR at D0. Additionally, the bicistronic miR-1/133 (Kusakabe et al, 2013), which has been implicated in muscle development and regeneration (Li et al, 2013;Mitchelson and Qin, 2015;Yin et al, 2008), was also upregulated during OS regeneration. In summary, the relative expression changes estimated by RNAseq for 9/15 mRNA transcripts (60%) were validated using qRT-PCR in at least one stage during regeneration.…”

Down-regulation of miR-133a as a poor prognosticator in non-small cell lung cancer

“…MiR-133a has two subtype, including miR-133a-1 and miR-133a-2, which are located on chromosomes 18q11.2, 20q13.33 (Mitchelson and Qin, 2015). In renal cell carcinoma, miR-133a could inhibit cell proliferation and invasion by regulating target gene transgelin-2 (TAGLN2) (Kawakami et al, 2012a).…”