MIR675

Summary

MIR675 (microRNA 675, HGNC:33351) is a microRNA gene on chromosome 11p15.5.

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 100033819 — 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:33351
Approved symbol	MIR675
Name	microRNA 675
Location	11p15.5
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-675
Ensembl gene	ENSG00000284010
Ensembl biotype	miRNA
OMIM	615509
Entrez	100033819
RNAcentral	URS0000691556 — miRNA, 73 nt, 13 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000390168

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000390168 — 1 exons

Exon	Start	End
ENSE00001507595	1996759	1996831

Expression profiles

Bgee: expression breadth broad, 18 present calls, max score 67.76.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
prefrontal cortex	UBERON:0000451	67.76	gold quality
blood	UBERON:0000178	64.88	gold quality
right frontal lobe	UBERON:0002810	62.12	gold quality
nucleus accumbens	UBERON:0001882	61.98	gold quality
anterior cingulate cortex	UBERON:0009835	58.03	gold quality
hypothalamus	UBERON:0001898	58.00	gold quality
caudate nucleus	UBERON:0001873	57.21	gold quality
Ammon’s horn	UBERON:0001954	56.62	gold quality
amygdala	UBERON:0001876	56.42	gold quality
cerebellar hemisphere	UBERON:0002245	56.03	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	55.94	gold quality
zone of skin	UBERON:0000014	55.78	gold quality
right hemisphere of cerebellum	UBERON:0014890	55.56	gold quality
substantia nigra	UBERON:0002038	54.31	gold quality
transverse colon	UBERON:0001157	52.72	gold quality
C1 segment of cervical spinal cord	UBERON:0006469	51.01	gold quality
skin of leg	UBERON:0001511	48.23	gold quality
putamen	UBERON:0001874	46.56	gold quality

Single-cell (SCXA)

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

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

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• H19-derived miR-675, through downregulation of its target RB, regulates colorectal cancer development. (PMID:19926638)
• Type II collagen expression is regulated by tissue-specific miR-675 in human articular chondrocytes (PMID:20529846)
• miR-139-3p, pmiR-675, and miR-335 allowed separation of adrenocortical adenomas from adrenocortical carcinomas (PMID:21471143)
• Chondrocytes, under hypoxic signaling, showed upregulation of H19, and miRNA-675 levels in close correlation. (PMID:22527881)
• H19 gene could inhibit human trophoblast cell proliferation via encoding miR-675 that targeted NOMO1 downregulation. (PMID:22832245)
• Studies focused on the role of microRNAs in cartilage have identified miR-140 and -675 as playing important roles in regulation of cartilage homeostasis. (PMID:23754477)
• Overexpression of miR-675 increases anchorage-independent growth capacity resulting in mesenchymal-to-epithelial transition, associated with a reduction in the expression of Twist1 in AFP-secreting hepatocellular carcinoma (PMID:23864307)
• miR-675 derived from keratinocytes could be involved in H19-stimulated melanogenesis using MITF as a target of miR-675 (PMID:24335901)
• miR-675 was positively expressed with H19 and was a pivotal mediator in H19-induced gastric cancer cell growth promotion. Subsequently, the tumor suppressor Runt Domain Transcription Factor1 (RUNX1) was confirmed to be a direct target of miR-675. (PMID:24388988)
• H19 regulates glioma development by driving miR-675 expression. (PMID:24466011)
• Findings suggest that inhibition of H19 long non-coding RNA (LncRNAH19) and miR-675 expression can promote migration and invasion of hepatocellular carcinoma (HCC) cells via AKT/GSK-3beta/Cdc25A signaling pathway. (PMID:24939300)
• The H19-miR-675 axis acts as a suppressor of prostate cancer metastasis via modulation of TGFBI expression. (PMID:24988946)
• miR-675 may serve as a potential therapeutic target of lung cancer (PMID:25219825)
• GPR55 was a direct target gene of miR-675-5p. (PMID:25889562)
• abnormal enhanced miR-675 expression increases bladder cancer growth by regulating p53 activation, and thus may be helpful in the development of effective treatment strategies for bladder cancer (PMID:26198047)
• H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b. (PMID:26353930)
• miR675 overexpression upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer. (PMID:26376677)
• results demonstrated that the novel pathway H19/miR-675/TGF-beta1/Smad3/HDAC regulates osteogenic differentiation of hMSCs and may serve as a potential target for enhancing bone formation in vivo. (PMID:26417995)
• ZO-1 and E-cad mRNAs are novel targets of miR-675.H19 interacts with HuR and regulates the intestinal epithelial barrier function via the H19-encoded miR-675. (PMID:26884465)
• the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in Gastric Cancer cells (PMID:26931432)
• miR-675-5p might play an oncogenic role in esophageal squamous cell carcinoma (ESCC) through RalBP1/RAC1/CDC42 signaling pathway by inhibiting REPS2 and might serve as a valuable prognostic biomarker and therapeutic target for ESCC patients. (PMID:27120794)
• The authors demonstrated, in vitro and in vivo, that miR675-5p over expression in normoxia is sufficient to induce a hypoxic moreover, miR675-5p depletion in low oxygen conditions, drastically abolishes hypoxic responses including angiogenesis. In addition, the data indicate an interaction of miR675-5p, HIF-1alpha mRNA and the RNA Binding Protein HuR in hypoxia-induced responses. (PMID:27279905)
• Data show that lncRNA H19 and H19-derived miR-675 were significantly downregulated in bone marrow mesenchymal stem cells (BMSCs) that were differentiating into adipocytes. (PMID:27349231)
• The expression level of Cdc25A was significantly increased (<0.05) after treatment with miR-675 mimics. (PMID:27644634)
• Results suggest that the strong correlation of H19 overexpression together with higher miR-675 and lymph node metastases could be useful predictive markers, indicating a potentially therapeutic strategy for HNSCC patients. (PMID:27994496)
• Transcriptional analyses on specimens from colon cancer patients confirmed, in vivo, the correlation between miR-675-5p over-expression and metastasis, thus identifying miR-675-5p as a new marker for colon cancer progression. (PMID:28061476)
• mir-675-5p regulates the progression of pancreatic cancer cells through the UBQLN1-ZEB1-mir200 pathway. (PMID:28212565)
• Increased miR-675 expression is associated with Non-small cell lung cancer progression through activation of NF-kappaB signaling pathway. (PMID:28719338)
• MiR-675 is a direct target to FADD and a functional component of the H19 which contributes to increased proliferation and apoptosis inhibition. (PMID:28848149)
• DLX3 regulates bone marrow mesenchymal stem cell proliferation through H19/miR-675 axis. (PMID:28963438)
• Expression levels of miR-675-5p in glioma tissues and cells were negatively correlated with RB1 expression at both mRNA and protein levels and promoted cell proliferation and migration. (PMID:28970140)
• MiR-675-5p is involved in hypoxia-mediated angiogenesis in mesenchymal stromal cells. (PMID:29111380)
• Study demonstrate that lncRNA H19 and its cognate miR-675 are inversely correlated with the amounts of ferritin heavy subunit in K562 cells, and that this phenomenon may be largely attributed to the increase in ROS production induced by the FHC silencing. (PMID:29544765)
• miR-675 regulates the odontogenic differentiation of human dental pulp cells by epigenetic regulating DLX3. (PMID:29604248)
• up regulation serum exosomal miR-675 and down regulation of CALN1 in tumor specimen was also found to be associated with the metastatic phenotype in osteosarcoma patients. (PMID:29626470)
• The results indicated that miR6753p may be involved in the progression of esophageal squamous cell cancer through regulating esophageal squamous cell cancer cell migration and invasion capacity via modulating epithelial mesenchymal transition markers (MMP2, MMP 9 and Ecadherin). (PMID:30106155)
• the results of the study demonstrated that miR6753p directly regulated the expression of DMTF1, which contributed to the further regulation of Colorectal cancer cell proliferation. (PMID:30592263)
• findings describe a relationship of the plasma levels of H19/miR-675 and NEAT1/miR-204 in the different breast cancer subtypes; in addition, they reveal an interplay between these lncRNAs and miRNAs in the regulatory network in MCF-7 cells (PMID:30803129)
• Results indicate the presence of a negative feedback loop in the pathological mechanism of diabetic nephropathy, where H19 downregulates the expression of VDR by upregulating the expression of miR-675, whereas reduced VDR expression subsequently reduced the expression of EGR1. (PMID:30815865)
• suggest that MU-DLX3 significantly inhibits hDPCs differentiation via H19/miR-675 axis and provides a new mechanism insight into how MU-DLX3 epigenetically alters H19 methylation status and expression contributes to dentin hypoplasia in Tricho-Dento-Osseous syndrome (PMID:31029881)

Cross-species orthologs

1 orthologs

Organism	Symbol	Gene ID
mus_musculus	Mir675	ENSMUSG00000076275

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.