MIR199B

Summary

MIR199B (microRNA 199b, HGNC:31573) is a microRNA gene on chromosome 9q34.11.

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 406978 — 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:31573
Approved symbol	MIR199B
Name	microRNA 199b
Location	9q34.11
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-199b
Ensembl gene	ENSG00000207581
Ensembl biotype	miRNA
OMIM	614791
Entrez	406978
RNAcentral	URS000075E907 — miRNA, 110 nt, 42 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384849

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384849 — 1 exons

Exon	Start	End
ENSE00001499856	128244721	128244830

Expression profiles

Bgee: expression breadth broad, 87 present calls, max score 83.08.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
olfactory segment of nasal mucosa	UBERON:0005386	83.08	gold quality
right hemisphere of cerebellum	UBERON:0014890	77.63	gold quality
cerebellar hemisphere	UBERON:0002245	76.62	gold quality
monocyte	CL:0000576	75.76	gold quality
blood	UBERON:0000178	75.62	gold quality
islet of Langerhans	UBERON:0000006	75.11	gold quality
bone marrow	UBERON:0002371	74.42	gold quality
endocervix	UBERON:0000458	72.90	gold quality
gastrocnemius	UBERON:0001388	72.71	gold quality
muscle of leg	UBERON:0001383	72.63	gold quality
endometrium	UBERON:0001295	72.62	gold quality
body of pancreas	UBERON:0001150	72.40	gold quality
fundus of stomach	UBERON:0001160	72.18	gold quality
stomach	UBERON:0000945	71.71	gold quality
placenta	UBERON:0001987	71.38	gold quality
body of stomach	UBERON:0001161	70.77	gold quality
urinary bladder	UBERON:0001255	70.04	gold quality
brain	UBERON:0000955	70.00	gold quality
heart left ventricle	UBERON:0002084	69.93	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	69.30	gold quality
heart	UBERON:0000948	69.29	gold quality
calcaneal tendon	UBERON:0003701	69.27	gold quality
ectocervix	UBERON:0012249	69.26	gold quality
Brodmann (1909) area 9	UBERON:0013540	69.19	gold quality
adrenal tissue	UBERON:0018303	69.15	gold quality
subcutaneous adipose tissue	UBERON:0002190	69.05	gold quality
lower esophagus muscularis layer	UBERON:0035833	69.04	gold quality
left ovary	UBERON:0002119	69.03	gold quality
lower esophagus	UBERON:0013473	69.03	gold quality
right atrium auricular region	UBERON:0006631	68.77	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.10

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): HES1

Literature-anchored findings (GeneRIF, showing 40)

• although miR-219-2 and 199b can be hemizygously lost in a significant proportion of CML cases with der(9q) deletion, they are unlikely to play a dominant role in this disease pathogenesis (PMID:18548097)
• miR-199b-5p expression correlates with metastasis spread; negative influence of miR-199b-5p on tumor growth and on the subset of medulloblastoma stem-cell-like cells (PMID:19308264)
• Decreased expression of microRNA-199b increases protein levels of SET (protein phosphatase 2A inhibitor) in human choriocarcinoma. (PMID:19900756)
• Study shows that miR-199b is a direct calcineurin/NFAT target gene that increases in expression in mouse and human heart failure, and targets the nuclear NFAT kinase dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1a (Dyrk1a) (PMID:21102440)
• Underexpressed miR-199b, which may be via the upregulation of Hif1alpha in hepatocellular carcinoma, is inversely correlated with survival and directly correlated with the malignant status of HCC patients. (PMID:21557766)
• Most AML patients had a significant decrease in miR-199b-5p levels with elevated PODXL & DDR1 expressions. Both PODXL & DDR1 are targets of miR-199b-5p. (PMID:22374871)
• Down-regulation of MIRN199B microRNA is associated with epigenetic modifications in medulloblastoma. (PMID:22411914)
• Explored deregulation of miRNAs targeting mTOR kinase (miR-99a, miR-100 and miR-199b) in endometrioid endometrial carcinoma. mTOR kinase expression was increased in EEC tissues and was accompanied by decreased expression of all three miRNAs. (PMID:22920721)
• The results suggest that miR-199b-5p may have the potential to be a novel important alternative therapeutic target for HER2-positive breast cancer. (PMID:23296799)
• indicate that expression of miR-23a, miR-27a, miR-199b, miR-221, and miR-223 by qRT-PCR can diagnose leukemia of ambiguous lineage as myeloid or lymphoid. (PMID:23444217)
• These results revealed that miR-199b-5p plays a role in Notch signaling in osteosarcoma (PMID:23574781)
• miR-199b expression level was decreased in prostate cancer while HIF-1alpha was significantly over-expressed. miR199b negatively regulated HIF-1alpha by targeting its 3’-untranslated region. (PMID:23594994)
• A functional link among the erythroid transcription factors GATA-1/NF-E2, miR-199b-5p in erythropoiesis. (PMID:24608802)
• Study suggests that the epigenetic silencing of miR-199b-5p during tumor progression is significantly associated with acquired chemoresistance in ovarian cancer through the activation of JAG1-Notch1 signaling. (PMID:24659709)
• Down-regulation of miR-199b associated with imatinib drug resistance in 9q34.1 deleted BCR/ABL positive chronic myeloid leukemia patients. (PMID:24680705)
• Among the miRNAomes, the abundant expression of the let-7 members was decreased in aborted decidua samples, whereas miR-199b-5p expression was consistently increased. (PMID:25747134)
• CCNL1 is the target gene of miR-199b-5p. (PMID:26043836)
• Increased Expression of microRNA-199b-5p Associates with invasion in Osteosarcoma. (PMID:26183062)
• miR-199a/b-3p functions as a tumor suppressor and has an important role in breast cancer metastasis through PAK4/MEK/ERK signaling pathway. (PMID:26399456)
• Overexpression of miR-199b-5p canceled the effects of atrasentan on klotho expression and apoptosis of renal tubular cells in both in vivo and in vitro. (PMID:26813039)
• There was a significant decrease of serum miR-199b expression level in patients with irritable bowel syndrome (IBS) and its different subtypes when compared with healthy controls with the highest level (1.9 +/- 0.53 log scale) in healthy controls and lowest one (0.71 +/- 0.27 log scale) in IBS with diarrhea (IBS-D) subtype. (PMID:27015896)
• Our findings clearly evidenced a novel and negative role of miR-199b in the regulation of SIRT1 in colorectal cancer cells (PMID:27145368)
• In conclusion, the present study revealed for the first time that miR-199b-5p plays a positive role in osteoblast differentiation. (PMID:27363340)
• Results show that miR-199b is a tumor suppressor emerges as a potential contributing mechanism to inhibit PP2A via PP2A inhibitor SET (SET) overexpression in metastatic colorectal cancer (mCRC). (PMID:27517624)
• Down-regulated miR-199b-5p in breast cancer patients is associated with malignant clinical characteristics. (PMID:27788476)
• These findings imply that miR-199b-5p performs an inhibitory role in osteogenic differentiation in ligamentum flavum cells by potentially targeting JAG1 and influencing the Notch signalling pathway. (PMID:27957826)
• Study found direct interactions between miR-199a/b-5p and the binding site of SNHG12 and shows that SNHG12 regulated hepatocellular carcinoma tumorigenesis and metastasis by targeting miR-199a/b-5p and the downstream targets in NF-kappaB pathway. (PMID:28073380)
• The data suggested that the +936C/T VEGFA variants significantly increased the risk of poorer stroke outcome by affecting the bindings of miR-199a and miR-199b to VEGFA mRNA at the rs30250340 polymorphic site. (PMID:28234972)
• Low miR199A1 expression is associated with bladder cancer. (PMID:28324890)
• Our data demonstrate that N-Cadherin was markedly overexpressed and miR-199b-5p was significantly downregulated in hepatocellular carcinoma (HCC). MiR-199b-5p exerts inhibitory effects on EMT, and directly targets N-cadherin in HCC, supporting the potential utility of miR-199b-5p as a promising strategy to treat HCC (PMID:28588321)
• Results showed that miR-199A1/A2/B were significantly reduced in patients with head and neck squamous cell carcinoma (HNSCC), and demonstrated that all members of the miR-199 family regulated ITGA3 in HNSCC cells. (PMID:28612520)
• The three well-conserved seed matched sites for miR-199a/b-5p in the discoidin domain receptor 1 (DDR1) 3’-UTR were targeted, and miRNA binding to at least two sites was required for DDR1 inhibition. (PMID:29429150)
• Study showed that miR-199 was downregulated in a hepatocarcinoma cell line (HCC) and, that miR-199 inhibited cell proliferation, invasion, and migration in HCC cells by targeting the 3’- UTR of RGS17. miR-199 may therefore be a novel diagnostic option for the treatment of patients with HCC. (PMID:29559347)
• miR-199b attenuated the inflammatory response at least partly through the GSK3beta/NF-kappaB signaling pathways in monocytes (PMID:29779167)
• MiR-199b-5p promotes cell proliferation, migration and suppresses apoptosis in cervical cancer cells. KLK10 is a direct target of miR-199b-5p. MiR-199b-5p expression is increased and positively correlated with KI-67 in human cervical cancer tissues and cell lines. (PMID:29807015)
• Therefore miR199b may serve as an oncogene in Wilms’ tumour (WT)progression by directly targeting RUNX3, thereby suggesting that the miR199b/RUNX3 axis may be a promising therapeutic target for patients with WT (PMID:29845298)
• Study results revealed that miR-199b-5p was significantly downregulated and negatively associated with parathyroid hormone levels in the sporadic but was upregulated in the hereditary parathyroid tumors proposing the potential role of miR-199b-5p as a novel biomarker for distinguishing these two types of parathyroid tumors. (PMID:30104706)
• profound effects of miR-133b and miR-199b on epithelial to mesenchymal transition (EMT) and renal fibrosis in diabetic OLETF rats and TGF-beta1-stimulated HK-2 cells. (PMID:30125566)
• this study revealed that miR-199b-5p functions as antioncogene miRNA in papillary thyroid carcinoma cells and that the miR-199b-5p/STON2 axis might be a potential treatment option for papillary thyroid carcinoma (PMID:30325582)
• miR-199b-5p plays a key role in cell invasion and metastasis and its expression correlated with overall survival in patients with head and neck squamous cell carcinoma (PMID:30411121)

Cross-species orthologs

3 orthologs

Organism	Symbol	Gene ID
danio_rerio	MIR199B	ENSDARG00000081800
danio_rerio	mir199-1a	ENSDARG00000083179
mus_musculus	Mir199b	ENSMUSG00000092807

Paralogs (2): MIR199A1 (ENSG00000207752), MIR199A2 (ENSG00000208024)

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.