MIR489

Summary

MIR489 (microRNA 489, HGNC:32074) is a microRNA gene on chromosome 7q21.3.

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.

Source: NCBI Gene 574442 — RefSeq curated summary.

At a glance

• Gene type: non-coding (miRNA) — no protein product; not a drug target. Variant/disease associations are omitted (they would be positional, from an overlapping protein-coding gene).

Identifiers

Gene identifiers

Field	Value
HGNC ID	HGNC:32074
Approved symbol	MIR489
Name	microRNA 489
Location	7q21.3
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-489
Ensembl gene	ENSG00000207656
Ensembl biotype	miRNA
OMIM	614523
Entrez	574442
RNAcentral	URS000075EA26 — miRNA, 84 nt, 7 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384923

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384923 — 1 exons

Exon	Start	End
ENSE00001499930	93483936	93484019

Expression profiles

Bgee: expression breadth broad, 12 present calls, max score 88.53.

Top tissues by expression

12 total, by Bgee expression score (0-100, higher = more expressed):

Tissue	Anatomy ID	Expression score	Quality
kidney	UBERON:0002113	88.53	gold quality
amygdala	UBERON:0001876	81.47	gold quality
lower esophagus muscularis layer	UBERON:0035833	70.98	gold quality
nucleus accumbens	UBERON:0001882	69.83	gold quality
ascending aorta	UBERON:0001496	66.95	gold quality
tibial artery	UBERON:0007610	66.70	gold quality
minor salivary gland	UBERON:0001830	63.66	gold quality
skin of abdomen	UBERON:0001416	63.50	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	62.81	gold quality
spleen	UBERON:0002106	59.98	gold quality
right frontal lobe	UBERON:0002810	54.88	gold quality
colon	UBERON:0001155	47.44	gold quality

Single-cell (SCXA)

Detected in 1 experiment(s), a significant marker in 0.

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.49

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 34)

• Identification of the tumour-suppressive miRNA miR-489 and its target, PTPN11, might provide new insights into the underlying molecular mechanisms of hypopharyngeal squamous cell carcinoma (PMID:20700123)
• miR-489 inhibited cisplatin resistance and cell growth, and promotes apoptosis by suppressing Akt3 expression. (PMID:24686007)
• Expression of miR-489 both inhibited Smad3 expression and Smad3 related epithelial mesenchymal transition properties in breast cancer cells. (PMID:24786471)
• this study described that miR-489 expression level was significantly reduced in lung cancer samples (n = 115) and cell lines. Abnormal expression of miR-489 regulated the cells invasion by binding SUZ12 3’-UTR in vitro. (PMID:25833694)
• increased miR-489 is an inhibitor of alveolar septation (PMID:26719145)
• In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. (PMID:26828271)
• miR-489 was expressed at significantly lower level in tumor tissues compared to the adjacent normal tissues. Downregulation of miR-489 in breast cancers was associated with aggressive tumor phenotypes. Overall, the results define a double-negative feedback loop involving miR-489 and the HER2-SHP2-MAPK signaling axis that can regulate breast cancer cell proliferation and tumor progression. (PMID:26918448)
• These data indicate that miR-489 could reverse the chemoresistance of breast cancer via the PI3K-Akt pathway by targeting SPIN1. (PMID:27171498)
• Our findings that miR-489 is a robust inhibitor of metastasis and a potential therapeutic target for treating pancreatic ductal adenocarcinomas (PMID:27793842)
• MiR-489-3p expression was downregulated in osteosarcoma cells especially in high metastatic potential cells and was also significantly decreased in metastatic lesions compared with their corresponding primary tumor samples. (PMID:27859625)
• MiR-489 targeted the mRNA 3’-untranslated region (3’-UTR) region of Jagged1 (JAG1). (PMID:28281959)
• miR-489 loss facilitates malignant phenotype of glioma cells probably via SPIN1-mediated PI3K/AKT pathway. (PMID:28666210)
• The mechanism study revealed that ASLNC02525, as an RNA sponge, broke the negative regulation of twist1 by hsa-miRNA-489-3p, and once ASLNC02525 was silenced, the highly expressed hsa-miRNA489-3p regained its regulation on twist1 and inhibited the proliferation and invasion. (PMID:28713968)
• Low miR489 expression is associated with recurrence and metastasis in colorectal cancer. (PMID:29071516)
• this study that miR-489-3p is highly expressed after spinal cord injury, and is involved in inhibition of neural cell proliferation, induction of apoptosis, and inhibition of neurite outgrowth. (PMID:29441872)
• The current study identifies autophagy as a novel pathway targeted by miR-489 and reports Unc-51 like autophagy activating kinase 1 (ULK1) and lysosomal protein transmembrane 4 beta (LAPTM4B) to be direct targets of miR-489. (PMID:29784669)
• Taken together, the findings of this study suggest that the miR381/miR489mediated expression of CUL4B modulates the proliferation and invasion of GC cells via the Wnt/betacatenin pathway, which indicates that the miR381/miR489CUL4B axis is critical in the control of GC tumourigenesis. (PMID:30483755)
• Our findings indicate that up-regulation of miR-489 could suppress pancreatic cancer (PC) cell proliferation and facilitate cell apoptosis through targeting AKT3. miR-489 and AKT3 might serve as potential targets in the therapy of PC. (PMID:31646811)
• MicroRNA-489 suppresses osteosarcoma invasion, migration and epithelial-to-mesenchymal transition by directly targeting NAA10. (PMID:31738038)
• miR-489 suppresses multiple myeloma cells growth through inhibition of LDHA-mediated aerobic glycolysis. (PMID:31872383)
• Knockdown of lncRNA MIR503HG suppresses proliferation and promotes apoptosis of non-small cell lung cancer cells by regulating miR-489-3p and miR-625-5p. (PMID:31983569)
• CREB1-induced lncRNA LEF1-AS1 contributes to colorectal cancer progression via the miR-489/DIAPH1 axis. (PMID:32248974)
• LncRNA SNHG5 regulates SOX4 expression through competitive binding to miR-489-3p in acute myeloid leukemia. (PMID:32266420)
• MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway. (PMID:32284070)
• MicroRNA-489 targets XIAP to inhibit the biological progression of ovarian cancer via regulating PI3K/Akt signaling pathway and epithelial-to-mesenchymal transition. (PMID:32373947)
• LncRNA SNHG1 contributes to the regulation of acute myeloid leukemia cell growth by modulating miR-489-3p/SOX12/Wnt/beta-catenin signaling. (PMID:32592199)
• MiR-489 aggravates H2O2-induced apoptosis of cardiomyocytes via inhibiting IGF1. (PMID:32880387)
• Effects of miR-489 targeting on SOX4 gene on proliferation and apoptosis of human hepatocellular carcinoma cells. (PMID:33402977)
• Upregulated circRNA hsa_circ_0071036 promotes tumourigenesis of pancreatic cancer by sponging miR-489 and predicts unfavorable characteristics and prognosis. (PMID:33507122)
• Ginsenoside Rg1 promoted the wound healing in diabetic foot ulcers via miR-489-3p/Sirt1 axis. (PMID:34507636)
• miR-489-3p promotes malignant progression of non-small cell lung cancer through the inactivation of Wnt/beta-catenin signaling pathway via regulating USP48. (PMID:35413838)
• Expression of Mir-489-3p as an Effective Marker of Poor Prognosis in Patients with Non-small-cell Lung Carcinoma. (PMID:35751896)
• miR-489 Confines Uncontrolled Estrogen Signaling through a Negative Feedback Mechanism and Regulates Tamoxifen Resistance in Breast Cancer. (PMID:35897675)
• Long noncoding RNA TPTEP1 suppresses diabetic retinopathy by reducing oxidative stress and targeting the miR-489-3p/NRF2 axis. (PMID:36795778)

Cross-species orthologs

2 orthologs

Organism	Symbol	Gene ID
danio_rerio	mir489	ENSDARG00000083308
mus_musculus	Mir489	ENSMUSG00000070107

Protein

Non-coding RNA — no protein product; not a drug target.

Function

No curated pathway, Gene-Ontology, or interaction data.

Disease & clinical

No curated disease, variant, or cancer-driver associations.

Drugs & pharmacology

No drug or pharmacology data — not an established drug target.