MIR326

Summary

MIR326 (microRNA 326, HGNC:31769) is a microRNA gene on chromosome 11q13.4.

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 442900 — 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:31769
Approved symbol	MIR326
Name	microRNA 326
Location	11q13.4
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-326
Ensembl gene	ENSG00000199090
Ensembl biotype	miRNA
OMIM	613755
Entrez	442900
RNAcentral	URS00006A8564 — miRNA, 95 nt, 29 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362220

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362220 — 1 exons

Exon	Start	End
ENSE00001436983	75335092	75335186

Expression profiles

Bgee: expression breadth broad, 59 present calls, max score 85.09.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
blood	UBERON:0000178	85.09	gold quality
calcaneal tendon	UBERON:0003701	82.36	gold quality
adrenal tissue	UBERON:0018303	79.82	gold quality
monocyte	CL:0000576	76.54	gold quality
liver	UBERON:0002107	75.82	gold quality
stomach	UBERON:0000945	75.30	gold quality
bone marrow	UBERON:0002371	72.69	gold quality
gastrocnemius	UBERON:0001388	72.54	gold quality
heart left ventricle	UBERON:0002084	72.04	gold quality
adult mammalian kidney	UBERON:0000082	71.57	gold quality
multicellular organism	UBERON:0000468	71.55	gold quality
myometrium	UBERON:0001296	70.86	gold quality
body of stomach	UBERON:0001161	70.21	gold quality
heart	UBERON:0000948	70.18	gold quality
transverse colon	UBERON:0001157	68.85	gold quality
granulocyte	CL:0000094	68.73	gold quality
endometrium	UBERON:0001295	68.53	gold quality
colon	UBERON:0001155	68.30	gold quality
body of pancreas	UBERON:0001150	67.87	gold quality
tibial artery	UBERON:0007610	67.85	gold quality
nucleus accumbens	UBERON:0001882	67.61	gold quality
left adrenal gland cortex	UBERON:0035825	67.51	gold quality
lower esophagus muscularis layer	UBERON:0035833	67.18	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	67.13	gold quality
intestine	UBERON:0000160	67.04	gold quality
right ovary	UBERON:0002118	67.04	gold quality
esophagus mucosa	UBERON:0002469	66.77	gold quality
body of uterus	UBERON:0009853	66.46	gold quality
Ammon’s horn	UBERON:0001954	66.33	gold quality
muscle layer of sigmoid colon	UBERON:0035805	66.19	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.85

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• identify a T(H)-17 cell-associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). (PMID:19838199)
• findings demonstrating the involvement of miR-326 in multidrug resistance mediated by MRP-1 provide new evidence about the roles of microRNAs determining MDR development of tumor cells (PMID:19883630)
• microRNA-326 partially mediated the toxic effects of Notch knockdown (PMID:19955368)
• human glioblastoma cells with high levels of PKM2 expressed lower levels of miR-326, suggestive of endogenous regulation of PKM2 by miR-326. (PMID:20667897)
• miR-326 is expressed at higher levels in T1D subjects with ongoing islet autoimmunity, similar to what has been observed in multiple sclerosis. (PMID:22069274)
• miR-326 and PINP demonstrated a strong correlation with tumor burden. Our findings, taken together, indicate that miR-326 could potentially serve as a novel biochemical marker for monitoring bone metastatic progression (PMID:23142363)
• results suggest that miR-326 is an important candidate tumor suppressor, and its down-regulated expression may contribute to glioma progression. (PMID:23292865)
• results demonstrates that miR-326, miR-130a, miR-155, miR-210 and the 4 miRNA-interactions could serve as prognostic and predictive markers for survival of GBM patients (PMID:23302469)
• downregulation of miR-326 may be a possible mechanism for unrestricted activation of Smo signal transducer of the oncogenic Hedgehog pathway in chronic myeloid leukemia (PMID:23341351)
• MIRN326 and NOB1 may play an important role in the development of glioma. (PMID:23869222)
• Human IPF lung specimens had markedly diminished miR-326 expression. (PMID:24279830)
• study provides empirical evidence suggesting that miR-326 and miR-9 may regulate dopaminergic signaling, and miR-326 and miR-9 may be considered as potential drug targets for the treatment of disorders involving abnormal DRD2 function (PMID:24675081)
• these results confirmed potential of miR-326 as a diagnostic biomarker to discriminate between relapsing and remitting phases of multiple sclerosis disease. (PMID:24792898)
• The levels of expression of 25 miRNA remained high and ten of these miRNA showed different expression from that at day 0. (PMID:24960647)
• MiR-326 as a negative regulator of HDAC3. (PMID:25138213)
• miR-326 overexpression not only repressed SMO and downstream genes but also decreased the activity of the Hh pathway. Moreover, miR-326 overexpression decreased self-renewal and stemness and partially prompted differentiation in U251 tumor stem cells. (PMID:25173582)
• Mechanistic investigations showed that VEGF-C increased CTTN expression by downregulating Dicer-mediated maturation of miR326, thereby relieving the suppressive effect of miR326 on CTTN expression. (PMID:25205106)
• For selected miRNAs, namely miR-149, miR-148b, miR-326, and miR-520a-3p, we demonstrate the simultaneous downregulation of the ErbB3 receptor and multiple downstream signaling molecules. (PMID:25630670)
• In pancreatic ductal adenocarcinoma, high miR-326 expression prolongs survival likely via the decreasing invasive potential of cancer cells. (PMID:25742499)
• Downregulation of miR-326 inhibited tumor proliferation and tumor metastasis by directly targeting NOB1 in colorectal carcinoma. Upregulation of miR-326 in CRC cells was revealed to be associated with a feedback loop involving downregulation of the NOB1. (PMID:25760058)
• miR-326 targets antiapoptotic Bcl-xL and mediates apoptosis in human platelets. (PMID:25875481)
• Adam17, a target of Mir-326, promotes epithelial-mesenchymal transition-induced cells invasion in lung adenocarcinoma. (PMID:26111641)
• miR-133a and miR-326 downregulate the mRNA expression of Bcl-xl in HepG2 cells. (PMID:26239225)
• miR-326 overexpression was a poor prognostic marker for gastric cancer patients, and miR-326 served as a tumor suppressor in gastric cancer via directly regulating FSCN1. (PMID:26359764)
• miR326 has a putative binding site within the 3’untranslated region of NSBP1. miR326 overexpression inhibited NSCLC cell proliferation and invasion. (PMID:26548724)
• Low miR expression is associated with non-small-cell lung cancer. (PMID:26840018)
• Study found reduced miR-326 levels concomitant with elevated Ucn1 levels in Edinger-Westphal nucleus (EWcp) of depressed suicide completers and in the EWcp of depressed rats. In fully recovered rats, both serum and EWcp miR-326 levels rebounded to nonstressed levels. While downregulation of miR-326 levels in primary midbrain neurons enhanced Ucn1 expression levels, miR-326 overexpression selectively reduced its levels. (PMID:27045550)
• miR-326 can restore CDDP chemosensitivity in the human lung adenocarcinoma cells by targeting SP1, and HOTAIR upregulate the expression of miR-326 target gene SP1. (PMID:27460077)
• The expression of miR-326 was significantly decreased in the serum of osteosarcoma patients compared to health controls. (PMID:27723574)
• The proto-oncogene NOB1 as a direct target of miR-326.Low miR-326 expression in gastric cancer.miR-326 role in gastric cancer cell proliferation and G2/M arrest. (PMID:27733214)
• Study data strongly support an important role for miR-326 in enhancing the chemosensitivity of human glioma cells to curcumin. (PMID:27819521)
• These results show that multidrug resistant leukemia cell microparticle regulation of ABCC1 in recipient cells is governed by the transfer of both miR-326 and ABCB1 from donor cells (PMID:28050891)
• Our results identify a new molecular mechanism involving miR-326 and Arrb1 as regulators of Sonic hedgehog medulloblastoma Cancer stem cells . Specifically, low levels of Arrb1 and miR-326 trigger and maintain Hh/Gli signaling and self-renewal (PMID:28716052)
• demonstrate that miR-326 served as a tumor suppressor by targeting TWIST1, and may serve as a biomarker or therapeutic target for patients with EC. (PMID:28975990)
• Authors identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. (PMID:29115574)
• Ectopic expression of SNHG1 inhibited miR-326 expression in nucleus pulposus cells and promoted CCND1 expression. (PMID:29466672)
• miR-326 suppresses EKLF expression directly by targeting its 3’ UTR. In K562 cells, mir-326 overexpression reduced EKLF and increased gamma-globin production, while EKLF inhibition did the opposite. miR-326 expression is positively correlated with HbF levels in beta-thalassemia patients. (PMID:29601850)
• Low expression of miR326 is associated with drug resistance in pediatric acute lymphoblastic leukemia. (PMID:29630744)
• VEGF-C reduced miR-326 expression and increased cortactin expression through c-Src signaling, leading to enhanced cervical cancer invasiveness. (PMID:29658350)
• miR-155 and miR-326 are increased 24 hours after surgery in the rejected group com - pared to the non-rejected group, or non-transplanted group. Increased expression level of miRNAs in the rejected group compared to the non- transplanted group shows that these markers had specificity for transplantation. (PMID:29658868)

Cross-species orthologs

2 orthologs

Organism	Symbol	Gene ID
mus_musculus	Mir326	ENSMUSG00000065571
rattus_norvegicus	Mir326	ENSRNOG00000035506

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.