MIR194-2

Summary

MIR194-2 (microRNA 194-2, HGNC:31565) is a microRNA gene on chromosome 11q13.1.

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 406970 — 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:31565
Approved symbol	MIR194-2
Name	microRNA 194-2
Location	11q13.1
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-194-2
Ensembl gene	ENSG00000284155
Ensembl biotype	miRNA
OMIM	610941
Entrez	406970
RNAcentral	URS0000759DC6 — miRNA, 85 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384864

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384864 — 1 exons

Exon	Start	End
ENSE00001499871	64891355	64891439

Expression profiles

Bgee: expression breadth tissue_specific, 5 present calls, max score 70.41.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
blood	UBERON:0000178	70.41	gold quality
omental fat pad	UBERON:0010414	67.27	gold quality
esophagus mucosa	UBERON:0002469	63.87	gold quality
spleen	UBERON:0002106	49.96	gold quality
left testis	UBERON:0004533	31.63	silver quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.00

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• miR-194 was significantly down-regulated both in preeclampsia (p = 0.0001) and IUGR (p = 0.0304) (PMID:23639576)
• we showed that miR-194 have tumor suppressor effects on RCC by reducing the cellular migration and invasion abilities. (PMID:23715501)
• miR-194 is upregulated in cancer tissue and serum of patients with pancreatic ductal adenocarcinoma. (PMID:24398877)
• Results demonstrate that miR-194 affected the growth and metastasis of osteosarcoma cells both in vitro and in vivo suggesting that miR-194 functions as tumor suppressor gene. (PMID:25096247)
• miR-194, regulating the MAP4K4/c-Jun/MDM2 signaling pathway, might act as a tumor suppressor and serve as a novel target for CRC prevention and therapy. (PMID:25602366)
• miR-194 regulated the progression of hepatocellular carcinoma through directly inhibiting the expression of MAP4K4 (PMID:26722431)
• Inhibition of YAP1 strongly induced hepatocytic differentiation of progenitor cells and YAP1 overexpression reversed the miR-194-induced hepatocytic differentiation of progenitor cells. (PMID:26731713)
• We demonstrated that miR-194 up-regulation helps phenethyl isothiocyanate suppress prostate cancer PCa cell invasion, suggesting a new mechanism by which phenethyl isothiocyanate modulates PCa metastasis. (PMID:26820911)
• These findings suggested that miR-194 inhibits proliferation and metastasis and reverses cisplatin-resistance of non-small cell lung cancer cells (PMID:26909612)
• MiR-194 targets KDM5B to inhibit esophageal squamous cell carcinoma development and progression. (PMID:27480251)
• Targeting of SOCS2 by miR-194 resulted in derepression of the oncogenic kinases FLT3 and JAK2, leading to enhanced ERK and STAT3 signaling. (PMID:28011622)
• In skin from psoriasis patients, the effect of miR-194 on cell proliferation and differentiation was significantly reversed by overexpression of GRHL2. Moreover, the expression of miR-194 and GRHL2 was inversely correlated in psoriasis lesional skin. Taken together, our results suggest that miR-194 inhibits the proliferation and promotes the differentiation of keratinocytes through targeting GRHL2. (PMID:28040329)
• Circulating microRNA-194 regulated human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway. (PMID:28358423)
• The present study…identified miR-194 as predictive biomarker of response to preoperative chemoradiotherapy for locally advanced rectal cancer (PMID:28870889)
• MiR-194 increases the lipopolysaccharide-induced the inhibition of cell viability and increasing of the cell apoptosis by inhibition of NF-kappaB pathway in WI38 cells. (PMID:29131027)
• The inhibitory effect of miR-194 on the proliferation and migration of osteosarcoma cells was reversed by overexpressing CDH2, implicating that miR-194 inhibited osteosarcoma tumourigenesis by suppressing the expression of CDH2. (PMID:29518783)
• Overexpressed SOX2OT promoted cell proliferation and metastasis of gastric cancer (GC) cells (SGC-7901, TMK-1) and the phosphorylation of AKT2 as well, while knockdown of SOX2OT reversed these effects. Besides that, miR-194-5p was predicted to be a target of SOX2OT and decreased expression of miR-194-5p was observed in GC tissues and cell lines. (PMID:29782828)
• Study demonstrated that MiR-194 levels were significantly decreased in blood of aortic dissection patients who underwent deep hypothermia circulatory arrest (DHCA) and in neurons under hypothermia oxygen glucose deprivation. Upregulated miR-194 decreased neuronal viability after oxygen and glucose deprivation and re-oxygenation. These data highlight the role of miR-194 in mediating DHCA response by regulating SUMO2. (PMID:30232383)
• MiR-194 was subject to the modulation of H19, and both H19 and miR-194 could synthetically encourageepithelial-mesenchymal transition, proliferation and viability of colorectal adenocarcinoma cells. (PMID:30278464)
• Results show that miR-194 expression is decreased in clear cell kidney carcinoma and associated with larger tumor size, advanced TNM stage and poor prognosis. (PMID:30334578)
• miR-194 was highly expressed in gastric cancer (GC) tissues, whereas SUFU was downregulated in GC tissues and cell lines, thus suggesting that miR-194 may be a carcinogenic miRNA, whereas SUFU may act as a tumor suppressor. (PMID:30542715)
• Low expression of miR194 was observed in hypopharyngeal carcinoma (HPC) tissues, and increasing its expression led to the inhibition of cancer cell viability, migration and invasion in vitro. The study suggested that miR194 may serve as an antioncogene in HPC through its effects on the SMURF1 expression and the mTOR signaling pathway. (PMID:30720112)
• miR-194-5p, was significantly downregulated in intervertebral disc degeneration samples and could bind to the three prime untranslated regions (3’-UTRs) of both CUL4A and CUL4B, thereby downregulating their expression. (PMID:30945295)
• LINC00909 could act as a ceRNA to interact with miR-194 and thereby up-regulate the expression of MUC1-C. (PMID:31132669)
• MicroRNA-194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF-beta/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria. (PMID:31190349)
• miR-194 inhibits PTBP1 expression by binding to the 3’-UTR of PTBP1 mRNA, resulting in reduced CCND3 levels and hepatocellular carcinoma cell growth. (PMID:31301177)
• In liver fibrosis MiR-194 expression was notably lacking in activated hepatic stellate cells (HSCs) from both humans and mice. Overexpression of miR-194 suppressed HSCs cell proliferation by cell cycle arrest in G0/G1 phase. AKT2 was predicted to be a target of miR-194. Results suggest that miR-194 plays a protective role in liver cirrhosis by inhibiting the activation and proliferation of HSCs via AKT2 suppression. (PMID:31496625)
• Long noncoding RNA Unigene56159 promotes glioblastoma multiforme cell proliferation and invasion through negatively regulating microRNA1945p. (PMID:31789416)
• Upregulated microRNA-194 impairs stemness of cholangiocarcinoma cells through the Rho pathway via inhibition of ECT2. (PMID:31960990)
• Downregulation of serum miR-194 predicts poor prognosis in osteosarcoma patients. (PMID:32172218)
• Dying tumor cell-derived exosomal miR-194-5p potentiates survival and repopulation of tumor repopulating cells upon radiotherapy in pancreatic cancer. (PMID:32228703)
• miR-194-5p inhibits LPS-induced astrocytes activation by directly targeting neurexophilin 1. (PMID:32533463)
• miR-194-5p inhibits SLC40A1 expression to induce cisplatin resistance in ovarian cancer. (PMID:32534701)
• Circulating microRNA-194 and microRNA-1228 Could Predict Colon Cancer Proliferation via Phospho S6 Modulation. (PMID:32919420)
• miR-194-5p down-regulates tumor cell PD-L1 expression and promotes anti-tumor immunity in pancreatic cancer. (PMID:34098485)
• Long non-coding RNA H19 acts as a microRNA-194 sponge to inhibit the apoptosis and promote the proliferation of hypertrophic scar fibroblasts. (PMID:34310900)
• Serum miR-373-3p and miR-194-5p Are Associated with Early Tumor Progression during FOLFIRINOX Treatment in Pancreatic Cancer Patients: A Prospective Multicenter Study. (PMID:34681562)
• Down-Regulation of miR-194-5p for Predicting Metastasis in Breast Cancer Cells. (PMID:35008751)
• circFCHO2 promotes gastric cancer progression by activating the JAK1/STAT3 pathway via sponging miR-194-5p. (PMID:35708677)
• Hsa_circ_0000591 drives osteosarcoma glycolysis and progression by sequestering miR-194-5p and elevating HK2 expression. (PMID:36809521)

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.