MIR296

gene
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Also known as hsa-mir-296

Summary

MIR296 (microRNA 296, HGNC:31617) is a microRNA gene on chromosome 20q13.32.

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 407022 — 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

FieldValue
HGNC IDHGNC:31617
Approved symbolMIR296
NamemicroRNA 296
Location20q13.32
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-296
Ensembl geneENSG00000284040
Ensembl biotypemiRNA
OMIM610945
Entrez407022
RNAcentralURS00006F0310 — miRNA, 80 nt, 2 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385215

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385215 — 1 exons

ExonStartEnd
ENSE000015002215881761558817694

Expression profiles

Bgee: expression breadth tissue_specific, 9 present calls, max score 67.23.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
omental fat padUBERON:001041467.23gold quality
lower esophagus muscularis layerUBERON:003583364.65gold quality
skin of abdomenUBERON:000141662.80gold quality
anterior cingulate cortexUBERON:000983562.13gold quality
skin of legUBERON:000151161.28gold quality
ascending aortaUBERON:000149659.63gold quality
thoracic mammary glandUBERON:000520047.87gold quality
caudate nucleusUBERON:000187346.98gold quality
testisUBERON:000047342.63gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.00

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • Existence of an altered microRNA expression pattern in Parathyroid carcinomas together with a potential role of miR-296 as novel oncosuppressor gene in these neoplasia. (PMID:19926710)
  • MiR-296 might play important roles in the pathogenesis of esophageal cancer and considered as a potential target for this malignancy intervention. (PMID:20485139)
  • The data demonstrate the hWNK4 3’-UTR plays an enhancer role by crosstalking with the promoter, and miR-296 suppresses hWNK4 expression through targeting on its 3’-UTR in a cell-specific fashion. (PMID:20561597)
  • miR-296 regulates HMGA1 expression and is associated with prostate cancer growth and invasion (PMID:21138859)
  • miR-296 or Scrib levels predict tumor relapse in hepatocellular carcinoma patients (PMID:21643016)
  • miR-296 is frequently upregulated during immortalization of human cells and contributes to carcinogenesis by downregulation of p53-p21(WAF1) pathway. (PMID:21724611)
  • MiR-296-3p regulates cell growth and multi-drug resistance of human glioblastoma by targeting ether-a-go-go (EAG1). (PMID:22999387)
  • These results indicate that hsa-miR-296-5p inhibits enterovirus 71 replication by targeting the viral genome. (PMID:23468506)
  • miR-296-5p/SCRIB axis plays a role in breast carcinogenesis (PMID:24527800)
  • These results support miR-296-5p playing a tumor-suppressive role by targeting Pin1. (PMID:24915000)
  • This study indicates that miR-296-5p expression is associated with resistance to radiotherapy and tumor recurrence in early stage laryngeal squamous cell carcinoma. (PMID:26264462)
  • Study indicated that miR-296 regulated PLK1 expression and could function as a tumor suppressor in non-small cell lung cancer progression. (PMID:26549165)
  • We show that the chromatin remodeling protein HMGA1 functions as a downstream effector of these biological responses to miR-296-5p and regulates Sox2 expression, a master driver of cell stemness, by modifying chromatin architecture at the Sox2 promoter (PMID:26898758)
  • we demonstrate that NF2 negatively controls the invasiveness of Glioblastoma multiforme through YAP-dependent induction of CYR61/CCN1 and miR-296-3p. (PMID:26923924)
  • Collectively, these results implicate miR-296-5p as a potential cause of invasiveness in cancer and suggest it as a promising therapeutic target for glioblastomas. (PMID:27927008)
  • Studied the role and expression of MIR296 in the metastasis and epithelial-mesenchymal transition of colorectal cancer. Found MIR296 inhibited migration and invasion of tumor cells, as well as suppressed S100A4 abundance in tumor cells. (PMID:28209128)
  • miR296 is downregulated in tissue from patients with pancreatic cancer and pancreatic carcinoma cell lines. These findings suggested that it may function as a tumor suppressor via inhibiting the growth, migration and invasion of pancreatic cancer cells. AKT2 was validated as a direct target of miR296 in pancreatic cancer cells. (PMID:28534950)
  • miR2965p/AKT2 axis serves important roles in Hepatocellular carcinoma carcinogenesis and progression. (PMID:28586057)
  • data indicated that MMP-2/MMP-9 was coordinately targeted by two non-coding RNAs, miR-296-3p and FOXCUT, which were decreased, and tumor-suppressing factors in choroidal malignant melanoma (PMID:29260433)
  • These results reveal a novel mechanism by which miR-296-3p negatively regulated by nicotine directly targets MK2-induced Ras/Braf/Erk/Mek/c-Myc or PI3K/AKT/c-Myc signaling to stimulate its own expression and suppress NPC cell proliferation and metastasis. (PMID:29525743)
  • High miR-296-5p expression is significantly associated with squamous cell carcinoma of the lung. (PMID:30337605)
  • Study demonstrates that miR296 is downregulated in non-small cell lung cancer (NSCLC) patient samples and cell lines. Moreover, miR296 is shown to directly target SGLT2 promoter region. Collectively, data suggest that miR296 not only inhibits NSCLC by downregulating SGLT2 expression, but also acts as a novel regulator of aberrant lung cancer cells to limit lung cancer progression. (PMID:30365049)
  • The antitumor effect of miR296 in CRC are at least in part due to the inactivation of the RAC-alpha serine/threonine-protein kinase (AKT) signaling pathway induced by the suppression of ARRB1 expression. (PMID:30365090)
  • Overexpression of miR-296-5p suppressed cell proliferation, arrested cell cycle progression, and increased the healing rate of diabetic wounds both in vivo and in vitro (PMID:30467970)
  • MiR-296-5p suppresses papillary thyroid carcinoma cell growth via targeting PLK1. (PMID:30915753)
  • HANR promotes lymphangiogenesis of hepatocellular carcinoma via secreting miR-296 exosome and regulating EAG1/VEGFA signaling in HDLEC cells. (PMID:31127654)
  • MiR-296-3p may affect the proliferation and migration of non-small cell lung cancer cells via regulating RABL3. (PMID:31298353)
  • MiR-296-5p inhibits cell invasion and migration of esophageal squamous cell carcinoma by downregulating STAT3 signaling. (PMID:31298412)
  • Low miR296 expression is associated with triple-negative breast cancer progression. (PMID:31337246)
  • MicroRNA-296-5p Promotes Cell Invasion and Drug Resistance by Targeting Bcl2-Related Ovarian Killer, Leading to a Poor Prognosis in Pancreatic Cancer. (PMID:31563901)
  • Up-regulation of ZFAS1 indicates dismal prognosis for cholangiocarcinoma and promotes proliferation and metastasis by modulating USF1 via miR-296-5p. (PMID:31565837)
  • The expression of circ_0076305 was found to have positive correlation with STAT3, and circ_0076305 was validated to regulate STAT3 via targeting miR-296-5p. The present study illustrated that circ_0076305 regulated STAT3 expression and DDP resistance of NSCLC cells via sponging miR-296-5p. (PMID:31647948)
  • Inhibition of LncRNA FOXD3-AS1 suppresses the aggressive biological behaviors of thyroid cancer via elevating miR-296-5p and inactivating TGF-beta1/Smads signaling pathway. (PMID:31678422)
  • MiR-296 Promotes Osteoblast Differentiation by Upregulating Cbfal. (PMID:31694033)
  • Results showed that miR-296 could directly bind to SOX12 and inhibit its expression in clear cell renal cell carcinoma. However, miR-296 expression is also regulated by hsa_circ_001895 through direct binding to inhibit its expression. (PMID:31782868)
  • MicroRNA-296 functions as a tumor suppressor in breast cancer by targeting FGFR1 and regulating the Wnt/beta-catenin signaling pathway. (PMID:31841196)
  • Fusobacterium nucleatum promotes epithelial-mesenchymal transiton through regulation of the lncRNA MIR4435-2HG/miR-296-5p/Akt2/SNAI1 signaling pathway. (PMID:31997506)
  • Long non-coding RNA UCA1 modulates cell proliferation and apoptosis by regulating miR-296-3p/Myc axis in acute myeloid leukemia. (PMID:32286143)
  • miR-296-5p suppresses stem cell potency of hepatocellular carcinoma cells via regulating Brg1/Sall4 axis. (PMID:32320856)
  • miR2963p promotes the proliferation of glioblastoma cells by targeting ICAT. (PMID:32323769)

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.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.