MIR495

Summary

MIR495 (microRNA 495, HGNC:32085) is a microRNA gene on chromosome 14q32.31.

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 574453 — 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:32085
Approved symbol	MIR495
Name	microRNA 495
Location	14q32.31
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-495
Ensembl gene	ENSG00000207743
Ensembl biotype	miRNA
OMIM	615149
Entrez	574453
RNAcentral	URS000075C517 — miRNA, 82 nt, 18 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385010

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385010 — 1 exons

Exon	Start	End
ENSE00001500017	101033755	101033836

Expression profiles

Bgee: expression breadth broad, 25 present calls, max score 79.76.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
intestine	UBERON:0000160	79.76	gold quality
adrenal tissue	UBERON:0018303	79.71	gold quality
blood	UBERON:0000178	79.10	gold quality
colon	UBERON:0001155	79.10	gold quality
placenta	UBERON:0001987	75.76	gold quality
ascending aorta	UBERON:0001496	69.19	gold quality
putamen	UBERON:0001874	68.00	gold quality
caudate nucleus	UBERON:0001873	66.36	gold quality
right lobe of liver	UBERON:0001114	65.88	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	65.28	gold quality
Ammon’s horn	UBERON:0001954	65.26	gold quality
thoracic mammary gland	UBERON:0005200	64.90	gold quality
left adrenal gland	UBERON:0001234	64.60	gold quality
skin of abdomen	UBERON:0001416	64.30	gold quality
left ovary	UBERON:0002119	64.00	gold quality
esophagus mucosa	UBERON:0002469	62.61	gold quality
cerebellar hemisphere	UBERON:0002245	62.41	gold quality
pituitary gland	UBERON:0000007	60.71	gold quality
adenohypophysis	UBERON:0002196	60.47	gold quality
right hemisphere of cerebellum	UBERON:0014890	59.83	gold quality
right frontal lobe	UBERON:0002810	59.60	gold quality
substantia nigra	UBERON:0002038	57.41	gold quality
hypothalamus	UBERON:0001898	52.60	gold quality
stomach	UBERON:0000945	47.25	gold quality
left testis	UBERON:0004533	34.04	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.81

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• Data show that miR-495 expression was directly modulated by transcription factor E12/E47, and promotes oncogenesis via downregulation of E-cadherin and REDD1. (PMID:21258409)
• our findings suggest that miR-495 and miR-551a both act as tumor suppressors by targeting the PRL-3 oncogene and inhibiting gastric cancer cell migration and invasion. (PMID:22469786)
• miR-495 likely functions as a tumor suppressor in acute myeloid leukemia with MLL rearrangements. (PMID:23132946)
• Loss of microRNA-495 expression is associated with glioblastoma multiforme. (PMID:23594394)
• miR-495 regulates the multi-drug resistance by modulation of ATP7A expression in non-small cell lung cancer and miR-495 may serve as a potential biomarker for the treatment of multi-drug resistant non-small cell lung cancer patients with high ATP7A levels (PMID:24038379)
• Mir-495, mapped to the 14q32.31 locus, regulates proliferation, apoptosis, migration and invasion in metastatic prostate cancer cells. (PMID:24166498)
• Using western blotting and luciferase assays, MTA3 was identified as a target of miR-495 (PMID:24293376)
• Changes in the expression of miR-381 and miR-495 are inversely associated with the expression of the MDR1 gene and development of multi-drug resistance. (PMID:24303078)
• This study indicates that miR-495 directly targets Sox9, ultimately leading to the regulation of chondrogenic differentiation in human mesenchymal stem cells. (PMID:24654627)
• Data indicate that junctional adhesion molecule A (JAM-A) is a potential target of microRNA-495 {miR-495) in breast cancer cells. (PMID:25070379)
• Data show that in arterial endothelial cells, inhibition of miR-329, miR-487b, and miR-495 all led to increased cell proliferation by approximately 20%, 50%, and 35%, respectively, but inhibition of miR-494 did not affect endothelial cell proliferation. (PMID:25085941)
• MicroRNA-495 has a role in regulating the proliferation and apoptosis of human umbilical vein endothelial cells by targeting chemokine CCL2 (PMID:25466836)
• miR-495 methylation-associated silencing inhibits the migration and invasion of human gastric cancer cells by directly targeting PRL-3 (PMID:25475733)
• results identify miR-495 as a molecular switch involved in the orchestration of the Warburg effect in glioma cells via targeting the expression of Glut1. (PMID:25759932)
• miR-495 directly interacts with the Gfi1 3’UTR to regulate Gfi1 at a post-transcriptional level and the expression level of miR-495 is inversely correlated with the Gfi1 protein level in medulloblastoma specimens. (PMID:26160036)
• miR-495 acts as a tumour suppressor gene by targeting FOXC1 at the post-transcriptional level in endometrial cancer (PMID:26198045)
• Targeting miR-130a and miR-495 could be a potential therapeutics to recover RUNX3 expression under hypoxic conditions and in early tumorigenic progression. (PMID:26375442)
• Expression of miR-495 in prostate cancer cells significantly downregulated Akt and mTOR, which further inhibited cancer cell proliferation, migration, and invasion in vitro. (PMID:27031291)
• hsamiR495 was downregulated in glioma tissues and cell lines, and acts as a tumor suppressor gene in glioma via the negative regulation of MYB. (PMID:27220777)
• miR-495 may act as a tumor suppressor by targeting Akt1 in esophageal squamous cell carcinoma. (PMID:27323412)
• miR-495 represents a new target not only for promoting endothelial cells (EC) generation from human induced pluripotent stem cells (hiPSCs) but also for enhancing angiogenesis and engraftment of hiPSC-derived ECs in ischemic heart. (PMID:27538588)
• the association of three miRNA single nucleotide polymorphisms (miR-130bT>C, miR-200bT>C, and miR-495A>C) with ischemic stroke prevalence and post-stroke mortality, was investigated. (PMID:27603512)
• radiation significantly reduced the expression level of miR-495 in carcinoma cell lines. In summary, miR-495 may have promise as an adjuvant for tumor radiation therapy to decrease RIBEs involving the Sp1/eNOS pathway (PMID:27697751)
• PTEN, a well-defined tumor suppressor was identified to be a target gene of miR-495. Rescue experiments showed that enforced expression of PTEN impaired miR-495-mediated bladder cancer proliferation and invasion. (PMID:28069380)
• TSPAN12 promotes chemoresistance and proliferation of small cell lung carcinoma under the regulation of miR-495. (PMID:28302484)
• mir495 is down-regulated in lung tumor samples. mir495 interacts with 3’-UTR of GRP78. (PMID:28363780)
• This study suggests that pre-treatment with miR-495 before chemotherapy could improve the curative effect on MDR1-based multidrug resistance cancer. (PMID:28411377)
• We also showed that knockdown of urothelial carcinoma-associated 1 increased the p21 protein expression through regulating enhancer of zeste homolog 2. In addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR-495 (PMID:28466784)
• miR-495 can directly target 3’-UTR of STAT-3 mRNA and thereby decrease the expression of STAT-3 in MCF-7 and HCC1973 cells by Targetscan and Dual-luciferase assay. We further analyzed miR-495 promoter methylation by sodium bisulfite sequencing method , and found DNA methyltransferase inhibitor, 5-AzaC concomitantly upregulated expression of miR-495 and downregulated (PMID:28498478)
• Low miR495 expression is associated with osteosarcoma invasion. (PMID:28627703)
• Molecular mechanism studies confirmed that Bmi-1 mediated these effects of miR-495 on MSCs. Taken together, our data demonstrated that miR-495 induced senescence of MSCs may be involved in the pathogenesis of pre-eclampsia (PE) (PMID:28628915)
• The findings suggest that the functional loss or suppression of miR-495-3p triggers overexpression of multiple oncogenic EMs, and thereby contributes to malignant transformation and growth of gastric epithelial cells. (PMID:28991363)
• MiR-495 acted as a critical tumor suppressor. (PMID:29221726)
• Introduction of miR-495 directly targeted Annexin A3 to inhibit the invasion and epithelial-mesenchymal transition of colorectal cancer cells by up-regulating p53, and the down-regulation of Annexin A3 was essential for inhibiting the invasion and epithelial-mesenchymal transition of colorectal cancer cells by overexpressing miR-495. (PMID:29224019)
• Upregulation of miR-495 ameliorates the high glucose-induced inflammatory, cell differentiation and extracellular matrix accumulation of human CFs by modulating both the NF-kappaB and TGF-beta1/Smad signaling pathways through downregulation of NOD1 expression. (PMID:29760746)
• Results provide evidence that miR-495 is down-regulated by LUCAT1 in clear cell renal cell carcinoma (ccRCC) through direct binding. (PMID:29932248)
• Low miR495 expression is associated with radioresistance in nasopharyngeal carcinoma. (PMID:30015969)
• Role of mesenchymal stem cells exosomes derived microRNAs; miR-136, miR-494 and miR-495 in pre-eclampsia diagnosis and evaluation (PMID:30261165)
• Results revealed that the expression level of miR495 was decreased in patients with gastric cancer, and indicated that miR495 regulated gastric cancer cell apoptosis and migration through the PI3K/Akt/mTOR pathway. (PMID:30272336)
• MiR-495-3p was downregulated in multidrug resistance cell lines and cancer tissues. In addition, the overexpression of miR-495-3p inhibited the gastric cancer multidrug resistance in vitro and in vivo by targeting GRP78 and regulating the autophagy process. (PMID:30341283)

Cross-species orthologs

0 orthologs

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.