MIR145

Summary

MIR145 (microRNA 145, HGNC:31532) is a microRNA gene on chromosome 5q32.

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 406937 — 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:31532
Approved symbol	MIR145
Name	microRNA 145
Location	5q32
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-145, MIR-145
Ensembl gene	ENSG00000276365
Ensembl biotype	miRNA
OMIM	611795
Entrez	406937
RNAcentral	URS00004F4657 — miRNA, 88 nt, 46 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384967

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384967 — 1 exons

Exon	Start	End
ENSE00001499974	149430646	149430733

Expression profiles

Bgee: expression breadth ubiquitous, 117 present calls, max score 99.64.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
right coronary artery	UBERON:0001625	99.64	gold quality
mucosa of stomach	UBERON:0001199	99.39	gold quality
lower esophagus muscularis layer	UBERON:0035833	99.20	gold quality
lower esophagus	UBERON:0013473	99.15	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	98.95	gold quality
smooth muscle tissue	UBERON:0001135	98.63	gold quality
left uterine tube	UBERON:0001303	98.59	gold quality
tibial artery	UBERON:0007610	98.39	gold quality
popliteal artery	UBERON:0002250	98.38	gold quality
muscle layer of sigmoid colon	UBERON:0035805	98.22	gold quality
body of uterus	UBERON:0009853	97.66	gold quality
myometrium	UBERON:0001296	97.17	gold quality
left coronary artery	UBERON:0001626	97.05	gold quality
prostate gland	UBERON:0002367	96.95	gold quality
fundus of stomach	UBERON:0001160	96.54	gold quality
thoracic aorta	UBERON:0001515	96.30	gold quality
ascending aorta	UBERON:0001496	96.09	gold quality
colon	UBERON:0001155	95.95	gold quality
fallopian tube	UBERON:0003889	95.70	gold quality
uterus	UBERON:0000995	95.65	gold quality
intestine	UBERON:0000160	95.38	gold quality
right ovary	UBERON:0002118	95.26	gold quality
transverse colon	UBERON:0001157	94.72	gold quality
duodenum	UBERON:0002114	94.65	gold quality
right uterine tube	UBERON:0001302	94.64	gold quality
esophagus	UBERON:0001043	94.32	gold quality
small intestine Peyer’s patch	UBERON:0003454	94.21	gold quality
small intestine	UBERON:0002108	94.12	gold quality
urinary bladder	UBERON:0001255	93.93	gold quality
descending thoracic aorta	UBERON:0002345	93.89	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	2.31

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): CEBPB, EWSR1, FLI1, POU5F1, PPARA, PPARG, RELA, TP53

Literature-anchored findings (GeneRIF, showing 40)

• miR-143 and miR-145 may play a certain role in the development of colon and/or rectal cancers but not in progression of the disease. (PMID:19242066)
• miRNAs (miR-142-5p, -155, and -223) are overexpressed in biopsies in acute rejection of kidney transplants (PMID:19289845)
• Loss of miR-145 may provide a selective growth advantage for MCF-7 by targeting RTKN. (PMID:19360360)
• Data show that IGF-IR resistant to miR145 is not down-regulated by miR145 but fails to rescue colon cancer cells from growth inhibition, and indicate that down-regulation of IRS-1 plays a significant role in the tumor suppressor activity of miR145. (PMID:19391107)
• Increased miR-145 expression inhibits human embryonic stem cells self-renewal, represses expression of pluripotency genes, and induces lineage-restricted differentiation; loss of miR-145 impairs differentiation and elevates OCT4, SOX2, and KLF4. (PMID:19409607)
• Decreased expression of microRNA-145 is asociated with gastric cancers. (PMID:19439999)
• results suggest that hsa-miR-145 is a key player in protecting a cell against EGFR mutation; restoration of hsa-miR-145 successfully inhibits growth in lung adenocarcinoma cells with EGFR mutation (PMID:19493678)
• we described a tumor suppression function of miR-145 in breast cancer cell lines, and we linked miR-145 to TP53 and ER-alpha (PMID:19730444)
• MiR-145 targets involved in cell cycle and neuregulin pathways were significantly down-regulated in the metastatic context. (PMID:19843336)
• lowered expression in myelodysplastic syndrome with deletion of the long arm of chromosome 5 (del(5q)) (PMID:19898489)
• Reduction in miR-145 expression may provide bladder cancer cells with a selective advantage by inhibition of cell death otherwise triggered in malignant cells. (PMID:19915607)
• miR-145 inhibits not only tumor growth but also cell invasion and metastasis. (PMID:19996288)
• Findings suggest that miR-143 and -145 are important onco-related genes for the initiation step of colorectal tumor development and that the chemically modified synthetic miR-143 may be a candidate as an RNA medicine for colorectal tumor therapy. (PMID:20094072)
• study identifies and validates new cancer-relevant direct targets of miR-145 in colon cancer cells and hereby adds important mechanistic understanding of the tumor-suppressive functions of miR-145 (PMID:20098684)
• Results suggest that miRNAs -26a, -34a, -145, and let-7b may modulate expression of IFN-beta, thereby influencing innate immunity from the earliest responses to viral infection. (PMID:20130213)
• miR-145 and miR-133a function as tumour suppressors and directly regulate FSCN1 expression in bladder cancer. (PMID:20160723)
• demonstrated a role for miR-26a, miR-145 and miR-26a in TRAIL-induced apoptosis. (PMID:20230625)
• miR-21, miR-182 and let7-5a were over-expressed, and miR-145 and miR-155 were under-expressed in a breast, a prostate, and a glioblastoma cancer cell line. (PMID:20370992)
• EWS-FLI-1 and miRNA-145 function in a mutually repressive feedback loop and identify their common target gene, SOX2, in addition to miRNA145 itself, as key players in Ewing sarcoma family tumors cell differentiation and tumorigenicity (PMID:20382729)
• data demonstrate that the host gene can function as a primary miRNA transcript and suggest that the down-regulation of host gene expression caused the low-expression of its encoded microRNAs-143 and -145 in human cancer cell lines and in cancer tissues (PMID:20525177)
• Investigation of the mechanisms of inactivation of miR-145 through epigenetic pathways revealed significant DNA methylation of the miR-145 promoter region in prostate cancer cell lines (PMID:20588276)
• study reveals a previously unrecognized function of miR-145 in DFF45 processing, which may underlie crucial aspects of cancer biology (PMID:20687965)
• A highly conserved sequence 3’ to the pre-miR plays a crucial role in miR145 expression. (PMID:20717966)
• There was no relation between the expression of miRNA in hypoxic neuroblastoma cells and the amplification of MYCN. However, in all hypoxic neuroblastoma cell lines with MYCN not amplified, miR-145 was overexpressed. (PMID:20809117)
• these data identify JAM-A and fascin as novel targets of miR-145, firmly establishing a role for miR-145 in modulating breast cancer cell motility. (PMID:20818426)
• miR-145 inhibits proliferation of non-small cell lung cancer cells through c-Myc (PMID:21092188)
• miR145 levels definitely increase in differentiating cells and also in growth-arrested cells, even in the absence of differentiation; miR145 could be required either early or late during the differentiation process. (PMID:21111732)
• KRAS and RREB1 are targets of miR-143/miR-145, revealing a feed-forward mechanism that potentiates Ras signaling (PMID:21159816)
• These findings suggest that the deregulation of miRNAs plays an important role in the progression of esophageal squamous cell carcinoma (ESCC), and that both miR-143 and miR-145 might act as anti-oncomirs common to ESCC. (PMID:21218087)
• miR-145 expression suppresses cell proliferation, migration and invasion in prostate cancer by targeting fascin homolog 1 actin-bundling protein (PMID:21258769)
• MiR-145 exhibits inhibitory effects on cancer cell proliferation. (PMID:21289483)
• Downregulation of miR-145 is through DNA methylation and p53 mutation pathways in prostate cancer. (PMID:21349819)
• Downregulation of miR-145 is associated with esophageal squamous cell carcinoma. (PMID:21351259)
• SWAP70 may be a target of miR-145, and it might have a potential oncogenic function. (PMID:21360565)
• The high levels of expression of mature MIR145 were associated with recurrence of metastasis in ESCC patients (PMID:21453382)
• miR-145 can impair the proliferation of human lung adenocarcinoma-initiating cells by targeting OCT4 (PMID:21479367)
• MiR-145 can inhibit the proliferation of lung cancer stem cells in A549 cell line via down-regulating OCT4 expression. (PMID:21496429)
• miR-145 is downregulated in ulcerative colitis. (PMID:21557394)
• miRs-143 and -145 are associated with bone metastasis of prostate cancer (PMID:21647377)
• down-regulation of Kruppel-like factor-4 (KLF4) by microRNA-143/145 is critical for modulation of vascular smooth muscle cell phenotype by transforming growth factor-beta and bone morphogenetic protein 4. (PMID:21673106)

Cross-species orthologs

2 orthologs

Organism	Symbol	Gene ID
danio_rerio	mir145	ENSDARG00000083100
mus_musculus	Mir145a	ENSMUSG00000065592

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.