MIR129-2

Summary

MIR129-2 (microRNA 129-2, HGNC:31513) is a microRNA gene on chromosome 11p11.2.

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 406918 — 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:31513
Approved symbol	MIR129-2
Name	microRNA 129-2
Location	11p11.2
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-129-2
Ensembl gene	ENSG00000199077
Ensembl biotype	miRNA
OMIM	621205
Entrez	406918
RNAcentral	URS00006515A6 — miRNA, 90 nt, 13 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362207

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362207 — 1 exons

Exon	Start	End
ENSE00001436970	43581394	43581483

Expression profiles

Bgee: expression breadth broad, 16 present calls, max score 90.72.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
sural nerve	UBERON:0015488	90.72	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	73.49	gold quality
monocyte	CL:0000576	72.14	gold quality
right hemisphere of cerebellum	UBERON:0014890	69.55	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	68.73	gold quality
cerebellar hemisphere	UBERON:0002245	68.21	gold quality
right frontal lobe	UBERON:0002810	67.67	gold quality
left adrenal gland cortex	UBERON:0035825	67.47	gold quality
body of stomach	UBERON:0001161	66.15	gold quality
anterior cingulate cortex	UBERON:0009835	64.60	gold quality
caudate nucleus	UBERON:0001873	60.61	gold quality
spleen	UBERON:0002106	59.93	gold quality
C1 segment of cervical spinal cord	UBERON:0006469	55.61	gold quality
nucleus accumbens	UBERON:0001882	55.07	gold quality
left testis	UBERON:0004533	45.88	gold quality
corpus callosum	UBERON:0002336	45.41	silver quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.16

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• Results imply that the aberrant expression of SOX4 is caused by epigenetic repression of miR-129-2 in endometrial cancer. (PMID:19887623)
• up-regulation of SOX4 was inversely associated with the epigenetic silencing of miR-129-2 in gastric cancer, and restoration of miR-129-2 down-regulated SOX4 expression. (PMID:20331975)
• Overexpression of miR-129-2 in mouse lung epithelial cells results in significant G1 phase arrest that eventually leads to cell death and G1 phase arrest in multiple human lung adenocarcinoma cell lines. (PMID:20404570)
• The expression of VCP was directly regulated by miR-129-5p and this regulation played an important role in the progression of hepatocellular carcinoma. (PMID:22536440)
• Report miR129-3p orchestrates both the centriole-to-basal body transition and subsequent cilia assembly through microRNA-mediated post-transcriptional regulation. (PMID:22684256)
• we disclose a miR-129-2(miR-335)/SOX4/Semaphorin-Plexin regulatory axis in the tumorigenesis of pancreatic cancer. (PMID:23251334)
• our results suggest that gastric juice miR-129-1-3p and miR-129-2-3p are potential biomarkers for the screening gastric cancer (PMID:23307240)
• Methylation-mediated repression of microRNA 129-2 enhances oncogenic SOX4 expression in hepatocellular carcinoma. (PMID:23402613)
• Epigenetic inactivation of the MIR129-2 is associated with hematological malignancies. (PMID:23406679)
• This study indicates that miR-129-2 methylation is highly accurate in distinguishing HCC patients from cirrhosis patients and healthy individuals, implying its potential utility as an early diagnostic marker for Hepatocellular carcinoma . (PMID:23580407)
• miR-129-2 suppresses proliferation and migration of esophageal carcinoma cells through downregulation of SOX4 expression. (PMID:23677061)
• MiR-129 has a unique potential as a tumor suppressor and a novel candidate for developing miR-129-based therapeutic strategies in colorectal cancer. (PMID:23744359)
• The results show that miR-129-2-3p and miR-129-5p, are down-regulated in gastric cancer cell lines and all of the mature products of miR-129 showed tumor suppressor activities. (PMID:24055727)
• miR-129-1-3p inhibits gastric cancer cell migration by targeting bradykinin receptor B2. (PMID:25008064)
• hyper-methylation of miR-129-5p CpG island might play important roles in the development of gastric cancer chemo-resistance by targeting MDR related ABC transporters (PMID:25344911)
• targeting miR-129-5p/VCP signaling pathway may serve as a therapeutic strategy for osteosarcoma management (PMID:25566966)
• miR-129, EGFR, and MMP9 appear to be promising therapeutic targets for preventing the metastasis of non-small cell lung cancer (PMID:25716201)
• In ovarian cancer cells, miR-129-5p, directly represses TAZ expression, leading to the inactivation of TEA domain transcription, and the downregulation of Hippo downstream genes, connective tissue growth factor and Cyclin A. (PMID:25895125)
• Taken together, our findings indicate an important role for miR-129-5p in the molecular etiology of invasive HCC and suggest that miR-129-5p could have potential therapeutic applications in HCC. (PMID:25912876)
• Results showed that MIR219-2, MIR663b and MIR1237 were transcriptionally silenced by DNA hypermethylation in human gastric cancer cell lines. (PMID:26043902)
• These findings strongly suggest that miR-129 is a tumour suppressive miRNA, playing important roles in the development and progression of human lung cancer. (PMID:26081366)
• we find that miR-129-5p suppresses breast cancer development and progression (PMID:26460733)
• observed a positive correlation between the hypermethylation of MIR-129-2 and the up-regulation of the RASSF1(A) and GPX1 genes in BC (PMID:26519551)
• miR-129 is significantly downregulated in prostate cancer patients and multivariate analysis confirmed that miR-129 is a novel independent prognostic factor for prostate cancer. (PMID:26823749)
• In tissues of prostate cancer patients, low CP110 and high miR-129-3p expression levels correlated with metastasi (PMID:26918338)
• downregulation of miR-129-2 results in BCL2L2 overexpression and disease progression in breast cancer patients. (PMID:26935022)
• Expression of miRNA-129-2-3p was upregulated in cortical brain tissue and plasma samples from patients with refractory temporal lobe epilepsy, but miR-935 not. Plasma miRNA-129-2-3p has great potential as a non-invasive biomarker for early detection and clinical evaluation of refractory temporal lobe epilepsy. (PMID:27689807)
• the potential roles of miR-129 as biomarkers for cancer diagnosis and prognosis, and promising tools for cancer treatment, are reviewed. (PMID:27802440)
• methylation frequency of miR-129-2 and miR-9-1 was significantly elevated in clear cell renal cell carcinoma (PMID:28251969)
• MALAT1 promoted osteosarcoma cell growth through inhibition of miR-142-3p or miR-129-5p and by targeting HMGB1. (PMID:28346809)
• Data show that suberoylanilide hydroxamic acid (SAHA) induced apoptosis via the down-regulation thioredoxin1 (Trx1), which was regulated by microRNA miR-129-5p. (PMID:28667779)
• his study demonstrates that miR129-5p is a sensitive and specific biomarker for heart failure in univentricular heart disease independent of ventricular morphology or stage of palliation. (PMID:28859128)
• The expression levels of miR-129-2 was observed to be elevated in patients with low expression of progesterone receptor in the Cancer Genome Atlas cohort. (PMID:28876975)
• PCAT-1 repressed inhibitory effect of miR-129-5p and reverse high mobility group box 1 (HMGB1) expression, a target gene of miR-129-5p. (PMID:28931210)
• MiR-129 is reduced in prostate cancer and is associated with the development and proliferation of prostate cancer. (PMID:29035829)
• MALAT1/miR-129-5p/HMGB1 axis could be provided as an important prognostic biomarker in colon cancer development. (PMID:29226325)
• The reexpression of miR1295p suppressed the cell proliferation, migration and invasion of OS cells. In addition, ROCK1 was confirmed as a direct target of miR1295p. (PMID:29328417)
• The high expression level of circulating miR-129 in the tissue and blood samples of colorectal cancer patients contributes to aberrant colon cancer cell proliferation and migration mainly by targeting estrogen receptor beta. (PMID:29441863)
• This study elaborated a novel UCA1/miR-129/ABCB1 regulatory axis underlying paclitaxel resistance of ovarian cancer cells. (PMID:29777711)
• miR-129 inhibited neuroblastoma growth and potentiated chemosensitivity by targeting MYO10 (PMID:29864913)

Cross-species orthologs

3 orthologs

Organism	Symbol	Gene ID
danio_rerio	mir129-2b	ENSDARG00000082458
danio_rerio	dre-mir-129-2	ENSDARG00000083082
mus_musculus	Mir129b	ENSMUSG00000106336

Paralogs (1): MIR129-1 (ENSG00000207705)

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.