MIR106A

Summary

MIR106A (microRNA 106a, HGNC:31494) is a microRNA gene on chromosome Xq26.2.

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 406899 — 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:31494
Approved symbol	MIR106A
Name	microRNA 106a
Location	Xq26.2
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-106a
Ensembl gene	ENSG00000284157
Ensembl biotype	miRNA
OMIM	300792
Entrez	406899
RNAcentral	URS000039E1E1 — miRNA, 81 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384870

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384870 — 1 exons

Exon	Start	End
ENSE00001499877	134170198	134170278

Expression profiles

Top tissues by expression

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

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)

• IL-10 expression may be regulated by miR-106a, which is in turn transcriptionally regulated by Egr1 and Sp1 (PMID:19307576)
• identified four commonly regulated miRNAs, miR-17 down-regulated in all seven; miR-19b and miR-20a, down-regulated in six models; and miR-106a down-regulated in five models. (PMID:20089119)
• Results indicate that the detection of miR-106a and -17 in peripheral blood may be a novel tool for monitoring circulating tumor cells in patients with gastric cancers. (PMID:20349219)
• Low miR-106a is associated with lymph recurrence in squamous cell esophageal carcinoma. (PMID:20628822)
• The expression of miR-17-3p and miR-106a is regulated by TNFalpha and lipopolysaccharides in HeLa cells. (PMID:21370248)
• two miRNA clusters, 106a-363 and 302-367, have roles in somatic cell reprogramming (PMID:21454525)
• miR-106a can increase p53 expression via E2F1 inhibition. (PMID:21656380)
• miR-106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS. (PMID:22431000)
• Data indicate that MiR-106a inhibits the expression of transforming growth factor-beta receptor 2 (TGFBR2), leading to increased colorectal cancer (CRC) cell migration and invasion. (PMID:22912877)
• results suggest that miR-106a might have a regulatory role for Rb1 in sporadic colorectal cancer (PMID:23178825)
• The miR-106a regulates osteogenic and adipogenic lineage commitment of hADSCs by directly targeting BMP2, and subsequently decreased osteogenic TAZ, MSX2 and Runx2, and increased adipogenic C/EBPalpha and PPARgamma. (PMID:23399447)
• Low MiR-106a expression is associated with glioblastoma. (PMID:23416698)
• c-Myc-regulated members of the miR-1792 and miR-106a363 clusters inhibit trophoblast differentiation by repressing GCM1 and CYP19A1. (PMID:23438603)
• These findings demonstrate for the first time that miR-17, miR-20a, and miR-106a regulate SIRPalpha synthesis and SIRPalpha-mediated macrophage inflammatory responses in a redundant fashion. (PMID:23562609)
• These studies provide support for a pro-oncogenic role of the miR-106a~363 cluster in Ewing Sarcoma. (PMID:23638178)
• MiR-106a and miR-591 have important roles in conferring Paclitaxel resistance to ovarian cancer cells. (PMID:23807165)
• Loss of miR-106a expression is associated with breast cancer. (PMID:23857602)
• Mcl-1 was a direct target of miR-106a. (PMID:23904379)
• MicroRNA-106a induces multidrug resistance in gastric cancer by targeting RUNX3. (PMID:23932924)
• Fecal miR-106a is a good molecular marker to identify colorectal cancer patients from among those with negative immunochemical fecal occult blood test. (PMID:23950216)
• MIR-106a-5p functions as a tumor suppressor during the development of astrocytomas by targeting FASTK. (PMID:24013584)
• expression profiling of miRNAs in high-grade serous ovarian carcinoma indicated miR-106a and its family members were upregulated; findings suggest miR-106a can repress expression of the retinoblastoma family member RBL2 and miR-106a overexpression results in rapid tumor growth and poor differentiation (PMID:24045973)
• Decreased miR-106a in GBM tissues and conferred a poor survival of GBM patients. SLC2A3 was identified as a core target of miR-106a in GBM cells. (PMID:24124917)
• TIMP2 is a direct downstream target for miR-106a (PMID:24440352)
• miR-106a has an oncogenic role in pancreatic tumorigenesis by promoting cancer cell proliferation, epithelial-mesenchymal transition and invasion by targeting tissue inhibitors of metalloproteinase 2 (TIMP-2). (PMID:24444603)
• Knockdown of miR-20a/106a in glioma stem cells increased endogenous TIMP-2 protein abundance, thereby inhibiting glioma stem cell invasion. miR-20a/106a has a key role in glioma stem cell invasion. (PMID:24704830)
• The expression of miR-106a was found to be upregulated, and miR-143 and miR-125b levels were found to be downregulated in colorectal tumor tissues compared with the normal tissues. (PMID:24746948)
• the extent of miR-106a expression increased during the transition from atypical hyperplasia to advanced carcinoma and had already had positive signals in early precancerous lesions but negative signals in normal gastric mucosal epithelial cells. (PMID:25115709)
• MicroRNA-106a confers cisplatin resistance in non-small cell lung cancer A549 cells by targeting adenosine triphosphatase-binding cassette A1. (PMID:25339370)
• Overexpression of miRNA-106 is associated with melanoma. (PMID:25361006)
• our study suggested that upregulated expression of miR-106a by its promoter hypomethylation might contribute to the progression of HCC, which might be considered as a potentially effective biomarker and therapeutic approach in the future. (PMID:25510666)
• Our data indicate that miR-106a stabilizes H19 expression in early differentiation of muscle cells. (PMID:25531890)
• PDGF-D expression is associated with miR-106a and Twist1 in HCC patients (PMID:25760076)
• Study revealed that miR-106a played an important role in the development of drug resistance to cisplatin and gefitinib in glioma. (PMID:25950430)
• These results indicate that miR-106a* affects renal cell carcinoma (RCC) progression by targeting IRS-2 with suppression of the PI3K/Akt signaling pathway in RCC cells (PMID:26018509)
• this study suggested that miR-106a inhibited the growth and metastasis of NSCLC cells by decreasing PTEN expression. (PMID:26097565)
• The expression level of miR-106a in plasma of Gastric Cancer patients (9.479+/-5.595) was significantly up-regulated compared with healthy controls (2.594+/-2.329) (p<0.05), while a remarkable decline of miR- 106a expression was observed in plasma of Gastric Cancer patients after gastrectomy. (PMID:26179261)
• FER1L4 could exert a tumor suppressive impact on colon cancer, which, through suppressing miR-106a-5p expression, and depletion of FER1L4, alone or combined with overexpression of miR-106a-5p, is predictive of poor prognosis in colon cancer. (PMID:26224446)
• The study suggested that miR-106a is downregulated in PBMCs of CHB patients and that miR-106a may play an important role in CHB by targeting IL-8. (PMID:26265888)
• miR-106a* might play an anti-oncogenic role in esophageal carcinoma by regulating CACUL1 expression, which suggest miR-106a* as a new potential diagnostic and therapeutic target for esophageal carcinoma. (PMID:26314198)

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.