MIR216A

Summary

MIR216A (microRNA 216a, HGNC:31593) is a microRNA gene on chromosome 2p16.1.

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 406998 — 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:31593
Approved symbol	MIR216A
Name	microRNA 216a
Location	2p16.1
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-216, hsa-mir-216a
Ensembl gene	ENSG00000207798
Ensembl biotype	miRNA
OMIM	610944
Entrez	406998
RNAcentral	URS000013ABA3 — miRNA, 110 nt, 6 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385063

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385063 — 1 exons

Exon	Start	End
ENSE00001500069	55988950	55989059

Expression profiles

Bgee: expression breadth broad, 20 present calls, max score 80.21.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
lower esophagus muscularis layer	UBERON:0035833	80.21	gold quality
blood	UBERON:0000178	76.05	gold quality
ascending aorta	UBERON:0001496	73.45	gold quality
body of pancreas	UBERON:0001150	71.36	gold quality
stomach	UBERON:0000945	70.83	gold quality
tibial artery	UBERON:0007610	69.91	gold quality
right lobe of liver	UBERON:0001114	69.90	gold quality
body of stomach	UBERON:0001161	69.55	gold quality
transverse colon	UBERON:0001157	69.28	gold quality
tibial nerve	UBERON:0001323	68.46	gold quality
intestine	UBERON:0000160	67.72	gold quality
esophagus mucosa	UBERON:0002469	67.43	gold quality
multicellular organism	UBERON:0000468	66.62	gold quality
colon	UBERON:0001155	66.62	gold quality
muscle layer of sigmoid colon	UBERON:0035805	65.71	gold quality
skin of abdomen	UBERON:0001416	65.30	gold quality
vagina	UBERON:0000996	62.71	gold quality
spleen	UBERON:0002106	61.75	gold quality
right frontal lobe	UBERON:0002810	51.27	gold quality
left testis	UBERON:0004533	50.36	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.80

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• The current study discovered the up-regulation of miRNA-216a by the androgen pathway and a subsequent suppression of TSLC1 as a new mechanism for the androgen pathway in early hepatocarcinogenesis. (PMID:22392644)
• Urinary miR-216a expression correlates with the rate of renal function decline in chronic kidney disease. (PMID:22960330)
• miR-216a is involved in the tumorigenesis and development of pancreatic cancer. (PMID:23174591)
• MicroRNA-216a/217-induced epithelial-mesenchymal transition targets PTEN and SMAD7 to promote drug resistance and recurrence of liver cancer. (PMID:23471579)
• MiR-216a overexpression repressed BECN1 and ATG5 expression and the ox-LDL induced autophagy. (PMID:24481443)
• Results show that the expression of miR-148a and miR-216a is downregulated in pancreatic ductal adenocarcinoma. (PMID:24895996)
• Our findings suggest that miR216a is a cancer suppressor miRNA and that overexpression of miR216a is a novel non-small-cell lung cancer treatment strategy (PMID:24958806)
• The results provided evidence that miR-216a targeting JAK2 negatively regulated the development of pancreatic cancer cells and may be used to develop a miRNA-based therapeutic strategy against pancreatic cancer. (PMID:25220761)
• MicroRNA-216a inhibits the growth and metastasis of oral squamous cell carcinoma by targeting eIF4B. (PMID:25955794)
• the results demonstrated that miR216a enhanced the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy, suggesting a promising molecular target for improving the radiotherapy of pancreatic cancer (PMID:26134156)
• Data indicate that Janus kinase 2 (JAK2) was a microRNA-216a (miR-216a) gene target. (PMID:26149212)
• Our study demonstrates that CSE/H2S system is regulated by miR-216a, and regulates ABCA1-mediated cholesterol efflux and cholesterol levels through the PI3K/AKT pathway. (PMID:26772887)
• Study demonstrated that plasma miRNA-216a/b might serve as potential biomarkers for the diagnosis of esophageal squamous cell carcinoma (ESCC) and dysregulation of miRNA-216a/b might be involved in the progression of ESCC. (PMID:26989293)
• Observed a significant negative correlation between miR-216a and MALAT1 in pancreatic ductal adenocarcinoma (PDAC) tissues and adjacent normal tissues. In vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase. (PMID:28034748)
• Circulating miR-216a may serve as a potential biomarker for severe acute pancreatitis (PMID:28183420)
• Low miR216a expression is associated with tumor invasion and metastasis in colorectal cancer. (PMID:28213952)
• Findings suggest a tumor suppressor role for miR-216a in gliomas, which inhibits glioma cell proliferation, migration, and invasion by targeting LGR5. (PMID:28256193)
• A bioinformatics analysis and luciferase reporter assay identified Smad3 as a direct target gene of miR-216b, and Smad3 expression was reduced by miR-216b overexpression at both the mRNA and protein levels. (PMID:28356485)
• YB-1 expression promotes pancreatic cancer metastasis that is inhibited by microRNA-216a. (PMID:28782557)
• Results found miR-216a-3p expression down-regulated in colorectal cancer (CRC) tissues and cell lines and correlated with shorter overall survival in patients with CRC. MiR-216a-3p could directly bind to the 3’-UTR of COX-2 and ALOX5, respectively. MiR-216a-3p inversely regulates the protein levels of COX-2 and ALOX5 in CRC cell lines. Ectopic miR-216a-3p expression significantly suppressed CRC cell proliferation. (PMID:28786533)
• miR-216a-3p can promote gastric cancer cell proliferation, migration, and invasion via targeting RUNX1 and activating the NF-kappaB signaling pathway (PMID:28835317)
• CDK14 expression was closely associated with poor prognosis and overall survival of Osteosarcoma patients. miR-216a inhibits CDK14 expression by binding to the 3’-untranslated region of CDK14. (PMID:29022909)
• SNHG16 could serve as an oncogene that promotes tumor progression by acting as an endogenous ‘sponge’ to regulate miR-216A-5p/ZEB1 in cervical cancer. (PMID:29126969)
• Urinary miR-377 and miR-216a can be considered early biomarkers of nephropathy in pediatric type 1 diabetes. Their correlation with carotid intimal thickness provides insights on the subclinical atherosclerotic process that occurs in diabetic nephropathy. (PMID:29175120)
• HOTTIP increased the expression of anti-apoptotic factor BCL-2, another important target gene of miR-216a, and jointly enhanced chemoresistance of small cell lung cancer by regulating BCL-2. (PMID:29367594)
• miR-216a promotes endothelial senescence and inflammation as an endogenous inhibitor of Smad3/IkappaBalpha pathway. (PMID:29512862)
• upregulation of miR-216a, which targets JAK2, could induce neuroprotection against ischemic injury in vitro and in vivo, which provides a potential therapeutic target for ischemic stroke (PMID:29521586)
• The miR-216a level in cancer cells was negatively correlated with DANCR expression. (PMID:29651883)
• These findings provide clues regarding the role of miR-216a-5p as a tumor suppressor in uveal melanoma through the inhibition of HK2. (PMID:29763606)
• AEG-1 as a target gene of miR-216b action. (PMID:29787989)
• HOTTIP negatively regulates miR-216a-5p expression in prostate cancer. (PMID:29884766)
• The results verified that TERT was highly expressed in macrophages of human carotid atherosclerotic plaques. miR-216a was found to promote telomerase activation in macrophages by 4.5-fold (P=0.002) through the Smad3/NF-kappaB pathway. (PMID:29940270)
• miR-216a up-regulation is associated with cisplatin resistance in ovarian cancer and this effect is mediated by PTEN. STAT3 is a regulator of miR-216a Strategies that inhibit miR-216a is a potential strategy for overcoming the cisplatin resistance in ovarian cancer. (PMID:30061175)
• miR-216a levels were considerably lower in the airway smooth muscle (ASM) cells of asthmatic patients than in those of non-asthmatic individuals. Overexpression of miR-216a markedly suppressed cell proliferation and promoted cell apoptosis in ASM cells. JAK2 was identified as direct functional target of miR-216a, and the ectopic expression of JAK2 partially rescued the inhibitory effect of miR-216a in ASM cells. (PMID:30299194)
• DANCR also strongly suppressed hepatocellular carcinoma tumor growth in vivo via targeting miR-216a-5p and KLF12. (PMID:30430564)
• overexpression of Linc00518 contributed to the paclitaxel resistance in prostate cancer via sequestering miR-216b-5p. (PMID:30462844)
• Investigated the function of miR-216a-5p in asthma by creating a bronchial epithelial cell (16HBE) injury model using HO. A significantly elevation of HMGB1 protein expression and a reduction of miR-216a-5p expression were observed in children with asthma as well as in HO stimulated 16HBE cells. (PMID:30502088)
• Knockdown of miR-216a-3p induces differentiation of bone marrow mesenchymal stem cells into type II alveolar epithelial cells through Wnt/beta-catenin pathway, thereby alleviating neonatal respiratory distress syndrome. (PMID:30536330)
• High miR216a expression is associated with proliferation and invasion of hepatocellular carcinoma. (PMID:30556161)
• Serum microRNA-216a was significantly decreased in patients with breast cancer compared with healthy controls. MicroRNA-216a overexpression led to a decrease in cell proliferation and migration, as well as increases in apoptosis in MCF-7 cells. microRNA-216a suppressed Wnt and beta-catenin expression in MCF-7 cells and this effect was reversed by anti-microRNA-216a by promoting the Wnt/beta-catenin signaling pathway. (PMID:30864744)

Cross-species orthologs

2 orthologs

Organism	Symbol	Gene ID
mus_musculus	Mir216a	ENSMUSG00000065539
rattus_norvegicus	Mir216a	ENSRNOG00000035514

Paralogs (1): MIR216B (ENSG00000211520)

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.