MIR301A
gene geneOn this page
Also known as hsa-mir-301hsa-mir-301a
Summary
MIR301A (microRNA 301a, HGNC:31622) is a microRNA gene on chromosome 17q22.
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 407027 — 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:31622 |
| Approved symbol | MIR301A |
| Name | microRNA 301a |
| Location | 17q22 |
| Locus type | RNA, micro |
| Status | Approved |
| Aliases | hsa-mir-301, hsa-mir-301a |
| Ensembl gene | ENSG00000207996 |
| Ensembl biotype | miRNA |
| OMIM | 615675 |
| Entrez | 407027 |
| RNAcentral | URS0000759EFA — miRNA, 86 nt, 34 organism(s) |
Gene structure
Transcript identifiers
Ensembl transcripts: 1 — 1 miRNA
ENST00000385261
RefSeq mRNA: 0 — MANE Select: None
Canonical transcript exons
ENST00000385261 — 1 exons
| Exon | Start | End |
|---|---|---|
| ENSE00001500267 | 59151136 | 59151221 |
Expression profiles
Bgee: expression breadth broad, 74 present calls, max score 75.03.
Top tissues by expression
74 total, by Bgee expression score (0-100, higher = more expressed):
| Tissue | Anatomy ID | Expression score | Quality |
|---|---|---|---|
| kidney | UBERON:0002113 | 75.03 | gold quality |
| islet of Langerhans | UBERON:0000006 | 74.88 | gold quality |
| blood | UBERON:0000178 | 74.84 | gold quality |
| muscle of leg | UBERON:0001383 | 74.43 | gold quality |
| gastrocnemius | UBERON:0001388 | 73.98 | gold quality |
| heart left ventricle | UBERON:0002084 | 72.50 | gold quality |
| fundus of stomach | UBERON:0001160 | 72.38 | gold quality |
| endometrium | UBERON:0001295 | 72.18 | gold quality |
| calcaneal tendon | UBERON:0003701 | 72.09 | gold quality |
| heart | UBERON:0000948 | 69.62 | gold quality |
| Brodmann (1909) area 9 | UBERON:0013540 | 69.14 | gold quality |
| body of pancreas | UBERON:0001150 | 68.81 | gold quality |
| granulocyte | CL:0000094 | 68.53 | gold quality |
| transverse colon | UBERON:0001157 | 68.09 | gold quality |
| stomach | UBERON:0000945 | 68.06 | gold quality |
| putamen | UBERON:0001874 | 67.22 | gold quality |
| dorsolateral prefrontal cortex | UBERON:0009834 | 67.21 | gold quality |
| C1 segment of cervical spinal cord | UBERON:0006469 | 67.18 | gold quality |
| tibial artery | UBERON:0007610 | 66.93 | gold quality |
| lung | UBERON:0002048 | 66.86 | gold quality |
| amygdala | UBERON:0001876 | 66.77 | gold quality |
| esophagus mucosa | UBERON:0002469 | 66.50 | gold quality |
| body of stomach | UBERON:0001161 | 65.99 | gold quality |
| thoracic aorta | UBERON:0001515 | 65.70 | gold quality |
| intestine | UBERON:0000160 | 65.68 | gold quality |
| skin of abdomen | UBERON:0001416 | 65.43 | gold quality |
| esophagus | UBERON:0001043 | 65.29 | gold quality |
| small intestine | UBERON:0002108 | 65.14 | gold quality |
| colon | UBERON:0001155 | 65.02 | gold quality |
| lower esophagus muscularis layer | UBERON:0035833 | 64.80 | gold quality |
Single-cell (SCXA)
Detected in 1 experiment(s), a significant marker in 0.
| Experiment | Marker? | Max mean expression |
|---|---|---|
| E-ANND-3 | no | 0.63 |
Regulation
Is transcription factor: no
Literature-anchored findings (GeneRIF, showing 40)
- blocking of miR-301 in A549 cells leads to a decrease in the expression of the host gene, ska2. (PMID:20470754)
- PlGF-induced PAI-1 expression at early time points is post-transcriptionally regulated by two miRNAs, miR-30c and miR-301a. (PMID:21175428)
- MiR-301a is a candidate oncogene that targets the homeobox gene Gax in human hepatocellular carcinoma.The upregulated miR-301a plays an important role in promoting proliferation, migration, and invasion, and in inhibiting apoptosis of HCC cells. (PMID:22373864)
- miR-301a promotes pancreatic cancer progression by repressing Bim. (PMID:22628193)
- miR-301a is involved in cellular clone formation, migration, and invasion in vitro and may play an important role in the clinical progression and prognosis of gastric cancer. (PMID:23832550)
- The expression of miR-301a in UC-MSCs was regulated by TLRs, and miR-301a affected the cytokine secretion of UC-MSCs (PMID:24035358)
- Upregulated microRNA-301a in breast cancer promotes tumor metastasis by targeting PTEN and activating Wnt/beta-catenin signaling. (PMID:24315818)
- analysis of the molecular network specific to pulmonary hypertension (PH) predicted that the miR-130/301 family is a master regulator of cellular proliferation in PH via regulation of subordinate miRNA pathways with unexpected connections to one another (PMID:24960162)
- Expression of miR-301a was an independent prognostic factor for the survival of patients with triple-negative breast cancer. (PMID:25311065)
- microRNA-130/301 controls vasoconstriction in pulmonary hypertension (PMID:25505270)
- data indicated that miR-301a correlated with the metastatic and invasive ability in human colorectal cancers and miR-301a exerted its role as oncogene by targeting TGFBR2 (PMID:25551793)
- MiR-301a promotes Colorectal cancer progression by directly downregulating SOCS6 expression. (PMID:25591765)
- miR-301a reduced doxorubicin-induced cell apoptosis whereas anti-miR-301a enhanced apoptosis in osteosarcoma (OS) cells, suggesting that up-regulation of miR-301a contributed to chemoresistance of OS cells. (PMID:25727016)
- MiR-301a-3p functions as a novel oncogene in pancreatic ductal adenocarcinoma and the oncogenic activity may involve its inhibition of the target gene SMAD4 (PMID:26019136)
- MicroRNA301 might function as a potential diagnostic biomarker for HCC. (PMID:26191271)
- Data show that increased microRNA miR-301a expression is associated with decreased manganese superoxide dismutase (MnSOD) expression in pancreatic ductal adenocarcinoma (PDAC) specimens. (PMID:26384137)
- miR-301a promotes pancreatic cancer growth by affecting MnSOD levels. (PMID:26384137)
- we show that fenofibrate, a PPAR-alpha agonist, increased the expression of miR-301a/miR-454 and SKA2 in human microvascular endothelial cell line (HMEC) cells; the former were responsible for reduced expression of ET-1 and PAI-1 (PMID:26460070)
- MiR-301a promotes cell proliferation and inhibits apoptosis by direct targeting TIMP2 in multiple myeloma (PMID:26464662)
- A YAP/TAZ-miR-130/301 molecular circuit exerts systems-level control of fibrosis in a network of human diseases and physiologic conditions (PMID:26667495)
- the data indicated that miR-301a-3p and Th17 cells were augmented in peripheral blood, which may play an important role in the process of Rheumatoid arthritis. (PMID:26782362)
- miR-301a/b-NDRG2 might be an important axis modulating autophagy and viability of prostate cancer cells under hypoxia. (PMID:26813459)
- Our results suggest that CNVs of miR-146a, miR-23a and miR-301a confer susceptibility to VKH syndrome, but not to BD. The contribution of miR-23a to VKH syndrome may be mediated by increasing the production of IL-6. (PMID:26818976)
- Results provided evidence that the expression levels of miR-301a in Ewing’s sarcoma (ES) cells were significantly increased and inversely correlated with PTEN expression levels, and that miR-301a played important roles in ES cell proliferation and tumorigenesis by targeting PTEN mRNA. (PMID:26846737)
- Loss of miR301 expression is associated with breast cancer. (PMID:26967567)
- data indicate that microRNA-301a functions as an oncogene in prostate cancer by directly targeting the p63 tumor suppressor leading to loss of E-cadherin and epithelial-mesenchymal transition (PMID:26990571)
- High miR301a expression is associated with glioma cell invasion. (PMID:27006177)
- Overexpressed miR-301a may increase CDC14A expression and promote cell proliferation and migration in osteosarcoma cells. Therefore, miR- 301a may be useful for osteosarcoma diagnosis and therapy. (PMID:27323075)
- MiR-301a and miR-301b are 2 hypoxia-responsive miRNAs that decrease autophagy of prostate cancer cells in hypoxia by targeting NDRG2. Through downregulating NDRG2, miR-301a and miR-301b can promote radioresistance of prostate cancer cells. (PMID:27327120)
- miR-301a may represent a novel prognostic indicator, a biomarker for the early detection of lymph node metastasis and a therapeutic target in NSCLC. (PMID:27461635)
- Among these miRNAs, only miR-181b-5p, miR-195-5p and miR-301a-3p expressions were found to be significantly different between the treatment-resistant group and the group responding well to the treatment. miRNAs may cause resistance by silencing the receptor genes of the drugs used for schizophrenia treatment. miR-181b-5p, miR-195-5p and miR-301a-3p may be candidate indicators (PMID:27552670)
- miR-301a may be used as a potential therapeutic target in the treatment of human malignant melanoma. (PMID:27855389)
- Low miR301-a expression is associated with chronic myelogenous leukemia. (PMID:28035415)
- In summary, we demonstrated that MIR301A expression was significantly increased in the IEC of patients with active IBD and CRC. MIR301A induced production of several proinflammatory cytokines (eg, IL1b, IL6, IL8, and TNF) by IEC and compromised intestinal barrier through inhibiting BTG1, which was significantly decreased in colonic mucosa of patients with active CD and UC. (PMID:28193514)
- Data show that the Japanese encephalitis virus (JEV)-induced expression of miR-301a led to inhibition of the production of the transcription factor IFN regulatory factor 1 (IRF1) and the signaling protein suppressor of cytokine signaling 5 (SOCS5). (PMID:28196914)
- anti-miR-301a-5p significantly blocked vancomycin-induced apoptosis and caspase activity in HK-2 cells, which was accompanied by downregulation of p53, and upregulation of MITF, HDGF and MDM-4 together. (PMID:29022913)
- Serum exosomal miR-301a expression may serve as a novel biomarker for glioma diagnosis and as a prognostic factor for advanced grade disease. (PMID:29076027)
- Data show that miR-301a suppressed the expression of cyclin-dependent kinase inhibitor p21 (p21) and Smad4 protein, and subsequently promoted G1/S cell cycle transition and cell proliferation in vitro and xenograft growth in nude mice in vivo. (PMID:29331421)
- These results suggest that analysing miR-301a expression in the breast tissue biopsy specimen at the time of diagnosis could have the potential to identify patients who are at high risk for developing metastasis as well as patients who might be candidates for active surveillance. (PMID:29396508)
- MiR-301a suppression abolished the protective functions of RP11-445H22.4 silencing on LPS-treated ATGC5 cells. (PMID:29414810)
Cross-species orthologs
2 orthologs
| Organism | Symbol | Gene ID |
|---|---|---|
| danio_rerio | dre-mir-301a-1 | ENSDARG00000083420 |
| rattus_norvegicus | Mir301a | ENSRNOG00000035586 |
Paralogs (2): MIR130A (ENSG00000208009), MIR301B (ENSG00000212102)
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.
Related Atlas pages
No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.