MIR362

Summary

MIR362 (microRNA 362, HGNC:32022) is a microRNA gene on chromosome Xp11.23.

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 574030 — 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:32022
Approved symbol	MIR362
Name	microRNA 362
Location	Xp11.23
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-362
Ensembl gene	ENSG00000208015
Ensembl biotype	miRNA
Entrez	574030
RNAcentral	URS000075A1A6 — miRNA, 65 nt, 4 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385280

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385280 — 1 exons

Exon	Start	End
ENSE00001500286	50008964	50009028

Expression profiles

Bgee: expression breadth broad, 18 present calls, max score 78.66.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
blood	UBERON:0000178	78.66	gold quality
monocyte	CL:0000576	78.49	gold quality
lung	UBERON:0002048	78.20	gold quality
sural nerve	UBERON:0015488	77.20	gold quality
heart	UBERON:0000948	76.69	gold quality
adrenal tissue	UBERON:0018303	76.68	gold quality
intestine	UBERON:0000160	73.86	gold quality
colon	UBERON:0001155	73.36	gold quality
stomach	UBERON:0000945	71.64	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	71.50	gold quality
body of stomach	UBERON:0001161	69.77	gold quality
adult mammalian kidney	UBERON:0000082	69.70	gold quality
muscle layer of sigmoid colon	UBERON:0035805	69.30	gold quality
omental fat pad	UBERON:0010414	66.58	gold quality
left ovary	UBERON:0002119	65.60	gold quality
subcutaneous adipose tissue	UBERON:0002190	63.92	gold quality
vagina	UBERON:0000996	63.00	gold quality
left testis	UBERON:0004533	42.03	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.33

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 34)

• miR-362 plays an important role in repressing the tumor suppressor CYLD and present a novel mechanism of miRNA-mediated NF-kappaB activation in gastric cancer. (PMID:24495516)
• High MicroRNA-362-5p promotes tumor growth and metastasis by targeting CYLD in hepatocellular carcinoma. (PMID:25449782)
• Results show that reduced methylation of miR-362 promoter can increase miR-362 expression leading to downregulation of the Tob2 target gene. miR-362 can increase cell proliferation via targeting Tob2 through the regulation of cell cycle progression. (PMID:25649327)
• These results suggested that microRNA-362-3p (miR-362-3p) or CD82 can be exploited as a new potential target for control of gastric cancers in the future. (PMID:25652145)
• The miR-362-5p promotes NK-cell function, at least in part, by the down-regulation of CYLD. (PMID:25909817)
• suggest that miR-362-5p suppresses neuroblastoma cell growth and motility, partially by targeting PI3K-C2beta (PMID:26073258)
• Evidence for a novel role for miR-362-3p and miR-329 as tumor suppressors. (PMID:26337669)
• Further experiments demonstrated that the overexpression of miR3623p resulted in decrease expression levels of nemo-like kinase (PMID:26647877)
• Taken together, our findings suggested that miR-362-3p inhibits the proliferation and migration of VSMCs by directly targeting ADAMTS1, which might provide novel insight into the molecular mechanisms underlying the action of miR-362-3p in atherosclerosis. (PMID:28890348)
• We therefore investigated the effects of CASC2 expression on NF-kappaB pathway activity. Ultimately, we determined that CASC2 regulates hepatocellular carcinoma cell activity by targeting miR-362-5p and thus inhibiting the NF-kappaB pathway (PMID:29319182)
• High miR-362-5p expression was associated with poorer overall survival implicating the oncogenic function in acute myeloid leukemia development. (PMID:29540187)
• miR-362-3p/Pax3 axis regulates cell viability, migration and invasion of HTR8/SVneo cells under hypoxia. (PMID:29665647)
• these findings shows that miR-362 promotes lung cancer metastasis through downregulation of Sema3A (PMID:30155491)
• The newly identified miR-362/SIX1 axis provides insight into the progression of Colorectal cancer. (PMID:31016902)
• MicroRNA-362-3p maintains EMT by regulating CD82. (PMID:31215741)
• miR-362-3p mediates the transcriptional regulation of hERG and is associated with survival in breast cancer. (PMID:31659098)
• Results identified high expression of miR-362 in HER2 TNBC subtype breast cancer. High miR-362 expression was correlated with shorter overall survival. (PMID:31929841)
• LncRNA FENDRR Upregulation Promotes Hepatic Carcinoma Cells Apoptosis by Targeting miR-362-5p Via NPR3 and p38-MAPK Pathway. (PMID:32251605)
• E2F1-induced overexpression of SBF2-AS1 promotes the expression of GRB2 by targeting miR-362-3p to facilitate the metastasis of NSCLC (PMID:32364763)
• Depletion of lncRNA MALAT1 inhibited sunitinib resistance through regulating miR-362-3p-mediated G3BP1 in renal cell carcinoma. (PMID:32663095)
• MicroRNA-362 inhibits cell growth and metastasis in glioblastoma by targeting MAPK1. (PMID:32964983)
• miR-362-3p suppresses sinonasal squamous cell carcinoma progression via directly targeting pituitary tumor-transforming gene 1. (PMID:33148101)
• MiR-362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFbeta/Smad pathway. (PMID:33210473)
• miR-362-3p Targets Orosomucoid 1 to Promote Cell Proliferation, Restrain Cell Apoptosis and Thereby Mitigate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury. (PMID:33459949)
• microRNA-362-3p targets USP22 to retard retinoblastoma growth via reducing deubiquitination of LSD1. (PMID:33475455)
• MicroRNA-362 negatively and positively regulates SMAD4 expression in TGF-beta/SMAD signaling to suppress cell migration and invasion. (PMID:33746597)
• A two-miRNA signature of upregulated miR-185-5p and miR-362-5p as a blood biomarker for breast cancer. (PMID:33962174)
• MicroRNA-362-5p promotes the proliferation and inhibits apoptosis of trophoblast cells via targeting glutathione-disulfide reductase. (PMID:34107852)
• Positive natural selection of N6-methyladenosine on the RNAs of processed pseudogenes. (PMID:34120636)
• Alteration of miR-362-5p and miR-454-3p expression elicits diverse responses in breast cancer cell lines. (PMID:34727290)
• Long noncoding RNA NEAT1 promotes ferroptosis by modulating the miR-362-3p/MIOX axis as a ceRNA. (PMID:35338333)
• Regulation of Iron-Ion Transporter SLC11A2 by Three Identical miRNAs. (PMID:36047197)
• Circ-IGF1R Affects the Progression of Colorectal Cancer by Activating the miR-362-5p/HMGB3-Mediated Wnt/beta-Catenin Signal Pathway. (PMID:36542208)
• MiR362-3p Alleviates Osteosarcoma by Regulating the IL6ST/JAK2/STAT3 Pathway in Vivo and in Vitro. (PMID:39051528)

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.