MIR93

Summary

MIR93 (microRNA 93, HGNC:31645) is a microRNA gene on chromosome 7q22.1.

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 407050 — 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:31645
Approved symbol	MIR93
Name	microRNA 93
Location	7q22.1
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-93
Ensembl gene	ENSG00000207757
Ensembl biotype	miRNA
OMIM	612984
Entrez	407050
RNAcentral	URS00000DDD35 — miRNA, 80 nt, 4 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385024

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385024 — 1 exons

Exon	Start	End
ENSE00001500031	100093768	100093847

Expression profiles

Bgee: expression breadth ubiquitous, 112 present calls, max score 91.07.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
bone marrow	UBERON:0002371	91.07	gold quality
skeletal muscle tissue	UBERON:0001134	87.29	gold quality
granulocyte	CL:0000094	84.96	gold quality
endometrium	UBERON:0001295	82.45	gold quality
primordial germ cell in gonad	CL:0000670 ∩ UBERON:0000991	82.32	gold quality
adrenal tissue	UBERON:0018303	81.16	gold quality
sural nerve	UBERON:0015488	80.96	gold quality
blood	UBERON:0000178	78.87	gold quality
rectum	UBERON:0001052	77.22	gold quality
lymph node	UBERON:0000029	76.75	gold quality
placenta	UBERON:0001987	76.45	gold quality
monocyte	CL:0000576	75.92	gold quality
stomach	UBERON:0000945	75.79	gold quality
body of stomach	UBERON:0001161	75.36	gold quality
small intestine	UBERON:0002108	74.55	gold quality
muscle of leg	UBERON:0001383	74.54	gold quality
right adrenal gland	UBERON:0001233	74.12	gold quality
small intestine Peyer’s patch	UBERON:0003454	74.07	gold quality
olfactory segment of nasal mucosa	UBERON:0005386	73.97	gold quality
fundus of stomach	UBERON:0001160	73.96	gold quality
body of pancreas	UBERON:0001150	73.48	gold quality
skin of abdomen	UBERON:0001416	73.31	gold quality
uterus	UBERON:0000995	73.30	gold quality
left adrenal gland cortex	UBERON:0035825	72.46	gold quality
liver	UBERON:0002107	72.39	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	72.33	gold quality
intestine	UBERON:0000160	72.20	gold quality
zone of skin	UBERON:0000014	72.17	gold quality
right adrenal gland cortex	UBERON:0035827	72.13	gold quality
gastrocnemius	UBERON:0001388	72.08	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.83

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): SP7

Literature-anchored findings (GeneRIF, showing 40)

• The miR-106b-25 cluster, including miR-106b, miR-93, and miR-25, is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer. (PMID:18328430)
• findings implicate a miR-93/miR-130b-TP53INP1 axis that affects the proliferation and survival of HTLV-1-infected/transformed cells (PMID:18974142)
• Knock-down studies for the miR-106b-25 cluster, which includes miR-106b, miR-93 and miR-25, showed that the expression of the cluster is necessary for cell proliferation and for anchorage-independent growth (PMID:19486339)
• These results suggest that the three miRNAs are negative regulators of Fus1 expression in lung cancers. (PMID:19671678)
• Decreased expression of miRNA-9 modulating histone acetylation is associated with Waldenstrom macroglobulinemia. (PMID:20519629)
• miR-93 promotes the growth of, and angiogenesis in astrocytomas, by suppressing, at least in part, integrin-beta8 expression. (PMID:20956944)
• Induction of miR-93 expression and reduced p53 binding to p21 gene promoter account for loss of p21(sdi1) expression in senescent cells after DNA damage, suggesting a mechanism of in vivo carcinogenesis in aged tissue without repair arrest. (PMID:21402054)
• Findings demonstrate that miR-93 and miR-155 constitutively suppress AID translation in MCF-7 cells, suggesting widespread roles for these miRs in preventing genome cytidine deaminations, mutagenesis, and oncogenic transformation. (PMID:21831295)
• miR-93 overexpression seems to play an important role in osteosarcoma cell growth and invasion. (PMID:21959981)
• Data suggest that miR-93 expressed during differentiation may inhibit SW1116h cancer stem cell proliferation and colony formation. (PMID:22180714)
• miR-93 can directly target PTEN, and participates in the regulation of the AKT signaling pathway (PMID:22465665)
• miR-93/Sp7 function loop mediates osteoblast mineralization (PMID:22467200)
• study showed that microRNA-93 can inhibit tumorigenesis and reduce the recurrence of CRC; these findings may have potential clinical applications for predicting the recurrence of CRC (PMID:22581829)
• Enforced expression of mir-93 completely blocks tumor development in mammary fat pads and development of metastases following intracardiac injection in mouse xenografts (PMID:22685420)
• Reveal an important contribution for miR-93 in hepatocarcinogenesis and suggest a role for TGFBR2 and ITGB8 dysregulation in this process. (PMID:22773266)
• MicroRNAs miR-21a and miR-93 are down regulated in peripheral blood mononuclear cells (PBMCs) from patients with type 1 diabetes. (PMID:22999472)
• The miR-93 promoted tumor angiogenesis and metastasis by suppressing LATS2 expression. (PMID:23111389)
• Downregulation of miR-93 was significantly correlated with unfavorable clinicopathologic features and short overall survival in patients with colon cancer. (PMID:23354160)
• These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in women with polycystic ovary syndrome and in women with insulin resistance. (PMID:23493574)
• Ectopic expression of miR-9 strongly accelerates terminal myelopoiesis and promotes apoptosis in vitro and in vivo. (PMID:23509296)
• PPARdelta is regulated by miR-9 in monocytes. (PMID:23525285)
• Data indicate that miR-106b-25 cluster (miR-106b, miR-93 and miR-25) targets the 3’UTR of the beta-TRCP2 transcript and increases the expression of Snail. (PMID:23611780)
• The results showed that higher expressions of miR-9 and miR-200c in human breast cancers were associated with lymph node metastasis. (PMID:23617747)
• High MiR-93 expression is associated with metastasis and invasion of cervical carcinoma. (PMID:23679328)
• In human cell lines, MIR93 reduces levels of ATG16L1 and autophagy and prevents autophagy-dependent eradication of intracellular bacteria. This process also appears to be altered in colon tissues from patients with active Crohn’s disease. (PMID:24036151)
• Low DAB2 and high miR-93 expression levels correlate with poor patient survival in non-small cell lung cancer. (PMID:24037530)
• One carrying the same region with a mutated miR-93 site (PMID:24433094)
• miR-29c and miR-429, but not miR-93, may have a role in early stage non-small lung cancer (PMID:24523873)
• overexpression of miR-93 in FFPE tissues may serve as an indispensable source for biomarker discovery and validation in breast cancer patients (PMID:24606013)
• The present study reports an involvement of miR-93-mediated TGFbR2 down-regulation in NPC aggressiveness, thus giving extended insights into molecular mechanisms underlying cancer aggressiveness. (PMID:24606633)
• Genetic variation in MIR93 is associated with gastric cancer. (PMID:24643999)
• MicroRNA-93 was aberrantly over-expressed in glioma tissues and cell lines (PMID:24721397)
• Levels of miRNA-93, 190, and 200b were not significantly different in core biopsies of locally advanced breast cancer patients with different HER2 expressions. (PMID:24865188)
• Hypoxic stress decreased the miR-9 level in ARPE-19 cells, which increased the transcriptional level of SRPK-1, resulting in alternative splicing shift to pro-angiogenic isoforms of VEGF165 in human retinal pigment epithelial cells. (PMID:25007957)
• Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas (PMID:25064468)
• TGF-beta induced RBL2 expression through down-regulating miR-93 in renal cancer cells (PMID:25183046)
• miR-93 may be considered as a biomarker associated with the biological and clinical characteristics of human triple-negative breast cancer. (PMID:25238878)
• The expression of the miR-25/93/106b family may be regulated through mechanisms distinct from its host gene, MCM7 (PMID:25243570)
• miR-93-CCNG2 axis may be involved in Laryngeal squamous cell carcinoma proliferation and progression. (PMID:25309979)
• MiR-93 suppresses colorectal cancer development. (PMID:25371073)

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.