Abstract
RNA component of mitochondrial RNA processing endoribonuclease (RMRP) is a non-coding transcript firstly acknowledged for its association with the cartilage-hair hypoplasia (CHH) syndrome, a rare autosomal recessive condition. This transcript has been spotted in both nucleus and mitochondria. In addition to its role in the pathogenesis of CHH, RMRP participates in the pathogenesis of cancers. Independent studies in bladder cancer, colon cancer, hepatocellular carcinoma, lung cancer, breast carcinoma and multiple myeloma have confirmed the oncogenic effects of RMRP. Mechanistically, RMRP serves as a sponge for some miRNAs such as miR-206, miR-613, and miR-217. In addition to these miRNAs, expressions of tens of miRNAs have been altered following RMRP silencing, implying the vast extent of RMRP/miRNA network. In the present narrative review, we explain the role of RMRP in the development of cancers and some other non-malignant disorders.
Highlights
Protein-coding genes comprise a minor portion of the mammalian genome, it has been revealed that the vast majority of these genomes is transcribed at some level (Carninci et al, 2005; Birney et al, 2007)
Over-expression of RNA component of mitochondrial RNA processing endoribonuclease (RMRP) has been reported in numerous types of cancers such as those originated from bladder, colorectal, lung, breast and gastric tissues
Up-regulation of RMRP is a marker of poor prognosis in these types of cancers
Summary
Protein-coding genes comprise a minor portion of the mammalian genome, it has been revealed that the vast majority of these genomes is transcribed at some level (Carninci et al, 2005; Birney et al, 2007). In the bladder cancer cell lines, RMRP can enhance proliferation, migration potential and invasiveness of cells through modulating expression of miR-206 (Cao et al, 2019), a tumor suppressor miRNA that induces cell cycle arrest (Huang et al, 2016). Xenograft model of gastric cancer, RMRP silencing attenuated tumor growth via modulation of miR-206 expression (Shao et al, 2016).
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