MicroRNA 489 is a miRNA that in humans is encoded by the MIR489 gene.[1]
Function
microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. miR-489 acts as tumor suppressor miRNA in breast cancer by inhibiting various oncogenic signaling pathway. It has been demonstrated miR-489 target HER2 and LAPTM4b by directly binding to their 3'UTR. Role of miR-489 has been studied in autochatothus MMTV-Her2 mouse model.[2]
Wu H, Xiao Z, Zhang H, Wang K, Liu W, Hao Q (2014). "MiR-489 modulates cisplatin resistance in human ovarian cancer cells by targeting Akt3". Anticancer Drugs. 25 (7): 799–809. doi:10.1097/CAD.0000000000000107. PMID24686007.
Jiang L, He D, Yang D, Chen Z, Pan Q, Mao A, Cai Y, Li X, Xing H, Shi M, Chen Y, Bruce IC, Wang T, Jin L, Qi X, Hua D, Jin J, Ma X (2014). "MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway". FEBS Lett. 588 (11): 2009–15. doi:10.1016/j.febslet.2014.04.024. PMID24786471.
Patel Y, Soni M, Awagulerwitsch A, Kern MJ, Liu S, Shah N, Singh UP, Chen H (August 2018). "Overexpression of miR-489 derails mammary hierarchy structure and inhibits HER2/neu-induced tumorigenesis". Oncogene. doi:10.1038/s41388-018-0439-1. PMID30104710.