MIR372

gene
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Also known as hsa-mir-372

Summary

MIR372 (microRNA 372, HGNC:31786) is a microRNA gene on chromosome 19q13.42.

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 442917 — 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

FieldValue
HGNC IDHGNC:31786
Approved symbolMIR372
NamemicroRNA 372
Location19q13.42
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-372
Ensembl geneENSG00000199095
Ensembl biotypemiRNA
OMIM612044
Entrez442917
RNAcentralURS000075E430 — miRNA, 67 nt, 6 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362225

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362225 — 1 exons

ExonStartEnd
ENSE000014369885378789053787956

Expression profiles

Bgee: expression breadth tissue_specific, 1 present calls, max score 66.27.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
bloodUBERON:000017866.27gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.00

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • miRNA-372 and miRNA-373 have roles as oncogenes in testicular germ cell tumors (PMID:17695719)
  • Hsa-miR-302b and hsa-miR-372 regulate expression of a number of targets that influence reprogramming of human somatic cells. (PMID:21490602)
  • study revealed that miRNA (miRs-372/373) can promote HBV expression through a pathway involving the transcription factor (PMID:21608007)
  • Anti-oncogenic role of miR-372 may be through control of cell growth and cell cycle progression by down-regulating the cell cycle genes CDK2 and cyclin A1. (PMID:21646351)
  • Investigated the cellular mechanisms involved in miR-372-induced silencing, by conducting a comparative proteomic analysis of NSCLC CL 1-0 cells expressing miRNA-372 and/or vector only, and up- or downregulated proteins were further classified. (PMID:22451061)
  • High miR-372 expression was associated with synchronous liver metastasis in colorectal cancer. (PMID:22456107)
  • pri-miRNAs-371-373_ht2 [C-A-C] haplotype were more protective to hepatocellular carcinoma (HCC) occurrence in patients with HBV infection; the polymorphism of pri-miRNAs-371-373 was not associated with spontaneous HBV clearance (PMID:22848681)
  • Expression of miR-372 may significantly promote the cellular proliferation, invasion, and migration of hepatocellular carcinoma cell lines. (PMID:23291979)
  • miR-372 may act as an oncogenic miRNA in gliomas and could represent a potential regulator of aggressive development and a candidate prognostic marker for this malignancy. (PMID:23298385)
  • Targeted serum miRNA (TSmiR) test for diagnosis and follow-up of (testicular) germ cell cancer patients: a proof of principle. (PMID:24012110)
  • onco-miR-372-373 has a role in testicular germ cell tumours; its imprinted antisense transcript anti-miR-371-3 has a tumour suppressive role (PMID:24201333)
  • miR-372 suppressed the expression of ATAD2, which was highly expressed in HCC and exerted a proto-oncogene effect in hepatic carcinogenesis. (PMID:24552534)
  • YY1 regulated SQSTM1 expression through the epigenetic modulation of the transcription of MIR372 (microRNA 372) which was found to target SQSTM1 directly. (PMID:24991827)
  • Data show that miR-372 modulated the expression of phosphoprotein phosphatase PHLPP2 by directly targeting its 3’-untranslated region (3’-UTR) and that miR-372 expression was inversely correlated with PHLPP2 expression in glioma samples. (PMID:25160587)
  • Low MIRN372 expression is associated with nasopharyngeal carcinoma. (PMID:25265349)
  • Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma (PMID:25880458)
  • data demonstrated that serum or tissue miR-372 levels were significantly up-regulated in patients with colorectal cancer or colorectal precancerous lesions, compared to healthy control subjects or normal tissues (PMID:26179262)
  • MiR-372 seemed to function as a tumour suppressor in renal cell carcinoma progression by inhibiting the IGF2BP1 expression. (PMID:26332146)
  • A serum/CSF miRNA panel (miR-371a-3p, miR-372-3p, miR-373-3p and miR-367-3p) was sensitive and specific for diagnosing pediatric extracranial malignant GCT as well as detecting relapse, and distinguishing GCT vs. non-GCT intracranial neoplasms. (PMID:26671749)
  • Results demonstrated for the first time that miR-372 suppresses tumorigenesis and the development of endometrial carcinoma. (PMID:26673619)
  • These findings uncover a miR-372/let-7 axis regulating human primordial germ cell (PGC) specification. (PMID:27066911)
  • microRNA-372 suppresses migration and invasion by targeting p65 in human prostate cancer cells. (PMID:27673408)
  • this study found that miR-372 overexpressed in pros- tate cancer (PC) serum samples and its overexpression in two PC cell lines promoted cell proliferation and migration. (PMID:27730751)
  • Results show that miR-372 expression is inhibited by PCAT-14 by inducing methylation of its promoter. Simultaneously, miR-372 eliminates the effects of PCAT-14 on proliferation, invasion, and cell cycle in hepatocellular carcinoma cells. (PMID:28415780)
  • The upregulation of FGF9 or the downregulation of miR-372-3p substantially retarded lung squamous cell carcinoma (LSCC) cell growth, mitosis, and invasion. MiR-372-3p enhanced LSCC cell proliferation and invasion through inhibiting FGF9. (PMID:28440022)
  • miR-372 expression was significantly lower in ovarian carcinoma than normal ovarian tissues and benign tumors. miR-372 overexpression inhibited cell proliferation and promoted cell apoptosis. (PMID:28456593)
  • The present study indicates a novel evidence for JMJD2A in tumorigenesis by upregulating miR372 in liver cancer cells. (PMID:28467776)
  • Downregulation of ULK1 inhibited the overexpression effects of miR-372, and upregulation of ULK1 reversed the effects of overexpressed miR-372 in human pancreatic adenocarcinoma cells. (PMID:28677209)
  • The current study provides the first statistically convincing evidence that downregulation of miR-372 may occur in gallbladder cancer tissues, which may be associated with aggressive and progressive tumor behavior by affecting CLIC1 expression. (PMID:28944858)
  • The expression level of miR-372-3p was significantly lower in osteosarcoma cell lines in comparison with the normal human osteoblastic cell line and the miR-372-3p mimic enhanced the osteosarcoma proliferation and metastasis. (PMID:29364472)
  • miR-372 is a novel mechanism exploited by a subset of parathyroid tumor cells to partially decrease sensitivity to apoptosis, to increase PTH synthesis and to deregulate Wnt signaling. (PMID:29724878)
  • findings suggest that miR-372/373 enhance colorectal cancer cell stemness by repressing the expression of differentiation genes. (PMID:30171794)
  • High miR372 expression is associated with epithelial-mesenchymal transition in breast carcinoma by activating the Wnt pathway. (PMID:30570852)
  • miR-372 contributes to enhanced radiosensitivity while represses invasion and metastasis in nasopharyngeal carcinoma. (PMID:30656832)
  • it is found in our study that LncRNA FER1L4 expression is positively correlated with E2F1 mRNA expression. After knockdown of FER1L4 expression, E2F1 expression is significantly down-regulated, whereas the expression of miR-372 is significantly up-regulated; the up-regulation of miR-372 leads to significant down-regulation of FER1L4 and E2F1 expression (PMID:30887657)
  • AEBP1 expression is regulated by glucose, palmitate, and miR-372-3p, a pathway that has a role in the pathogenesis of hepatic fibrosis in nonalcoholic steatohepatitis (PMID:31299062)
  • The expression of HULC in serum exosomes and liver cancer tissues correlated with each other and the tumor-node-metastasis stage. Upregulation of HULC facilitated the secretion of exosomes from hepatocellular carcinoma cells. HULC repressed miR-372-3p expression. Rab11a was identified as a downstream target of miR-372-3p. miR-372-3p could directly bind both HULC and Rab11a. (PMID:31558873)
  • OSER1-AS1 acted as a ceRNA to sponge miR-372-3p, thereby positively regulating the Rab23 expression and ultimately acting as a tumor suppressor gene in hepatocellular carcinoma progression (PMID:31635804)
  • MiR-372-3p promotes tumor progression by targeting LATS2 in colorectal cancer. (PMID:31646563)
  • The microRNAs miR-302b and miR-372 regulate mitochondrial metabolism via the SLC25A12 transporter, which controls MAVS-mediated antiviral innate immunity. (PMID:31767682)

Cross-species orthologs

3 orthologs

OrganismSymbolGene ID
mus_musculusMir294ENSMUSG00000077903
mus_musculusMir291bENSMUSG00000078032
rattus_norvegicusrno-mir-295-1ENSRNOG00000082833

Paralogs (1): MIR371A (ENSG00000199031)

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.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.