| HGNC Family | Non-coding RNAs |
| Name | microRNA 299 |
| Description | 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. [provided by RefSeq, Sep 2009] |
| Summary |
{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐299 (miR‑299) has been identified as a potentially important tumor‐suppressive molecule in several malignancies. In metastatic prostate cancer, for example, miR‑299‐5p is among a cluster of miRNAs that is consistently downregulated in malignant cells compared with normal prostatic epithelial cells; this lower expression correlates with increased metastatic events and higher prostate‐specific antigen levels, suggesting that miR‑299 may help restrain cancer progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn glioblastoma, evidence points to an indirect regulatory circuitry, whereby the long noncoding RNA TUG1 is overexpressed and normally acts to suppress miR‑299 levels. Knockdown of TUG1 results in increased miR‑299 expression, which in turn downregulates vascular endothelial growth factor A (VEGFA) expression. This leads to a marked reduction in tumor‐induced endothelial proliferation, migration, and tube formation, implying that miR‑299 can inhibit key steps in angiogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn endometrial carcinoma, a similar relationship is observed. Elevated levels of TUG1 in tumor tissues are associated with suppressed miR‑299 (along with miR‑34a‑5p), and this suppression is linked to enhanced tumor progression. The inverse relationship between TUG1 and miR‑299 underscores the putative tumor‑suppressive function of miR‑299, suggesting that its loss may contribute to the oncogenic process."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nOutside of cancer, miR‑299 also appears to influence cell migration and invasion in placental development. In cases of severe pre‑eclampsia, miR‑299 is upregulated in placental tissues. Functional studies in trophoblast cells reveal that overexpression of miR‑299 suppresses both migration and invasion, an effect mediated in part by direct targeting of histone deacetylase 2 (HDAC2). These findings indicate a role for miR‑299 in modulating trophoblast behavior and placental formation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn hepatocellular carcinoma, miR‑299‑3p is significantly downregulated in tumor tissues compared with normal liver, and lower miR‑299‑3p levels are associated with aggressive tumor features such as larger size, venous infiltration, and poorer patient survival. Mechanistic studies have demonstrated that miR‑299‑3p suppresses cell migration, invasion, and proliferation by directly targeting Sirtuin‑5 (SIRT5), reinforcing its function as a tumor suppressor and highlighting its potential as a prognostic indicator and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "A Formosa, E K Markert, A M Lena, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MicroRNAs, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32.31 locus, regulate proliferation, apoptosis, migration and invasion in metastatic prostate cancer cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncogene (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/onc.2013.451"}], "href": "https://doi.org/10.1038/onc.2013.451"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24166498"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24166498"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "H Cai, X Liu, J Zheng, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA taurine upregulated 1 enhances tumor-induced angiogenesis through inhibiting microRNA-299 in human glioblastoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncogene (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/onc.2016.212"}], "href": "https://doi.org/10.1038/onc.2016.212"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27345398"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27345398"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Lifen Liu, Xin Chen, Ying Zhang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA TUG1 promotes endometrial cancer development via inhibiting miR-299 and miR-34a-5p."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncotarget (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.18632/oncotarget.15607"}], "href": "https://doi.org/10.18632/oncotarget.15607"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28404901"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28404901"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Yu Gao, Ruilian She, Qian Wang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Up-regulation of miR-299 suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting HDAC2 in pre-eclampsia."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biomed Pharmacother (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.biopha.2017.11.053"}], "href": "https://doi.org/10.1016/j.biopha.2017.11.053"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29145147"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29145147"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Shan Dang, Jian Zhou, Zongyan Wang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MiR-299-3p functions as a tumor suppressor via targeting Sirtuin 5 in hepatocellular carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biomed Pharmacother (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.biopha.2018.06.042"}], "href": "https://doi.org/10.1016/j.biopha.2018.06.042"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30170358"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30170358"}]}]}]}
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| Synonyms | MIR-299, MIRN299 |
| NCBI Gene ID | 407023 |
| API | |
| Download Associations | |
| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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MIR299 has 279 functional associations with biological entities spanning 6 categories (molecular profile, functional term, phrase or reference, chemical, disease, phenotype or trait, cell line, cell type or tissue, gene, protein or microRNA) extracted from 16 datasets.
Click the + buttons to view associations for MIR299 from the datasets below.
If available, associations are ranked by standardized value
| Dataset | Summary | |
|---|---|---|
| CCLE Cell Line Gene CNV Profiles | cell lines with high or low copy number of MIR299 gene relative to other cell lines from the CCLE Cell Line Gene CNV Profiles dataset. | |
| COSMIC Cell Line Gene CNV Profiles | cell lines with high or low copy number of MIR299 gene relative to other cell lines from the COSMIC Cell Line Gene CNV Profiles dataset. | |
| ENCODE Histone Modification Site Profiles | histone modification site profiles with high histone modification abundance at MIR299 gene from the ENCODE Histone Modification Site Profiles dataset. | |
| ENCODE Transcription Factor Binding Site Profiles | transcription factor binding site profiles with transcription factor binding evidence at the promoter of MIR299 gene from the ENCODE Transcription Factor Binding Site Profiles dataset. | |
| ENCODE Transcription Factor Targets | transcription factors binding the promoter of MIR299 gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset. | |
| GeneRIF Biological Term Annotations | biological terms co-occuring with MIR299 gene in literature-supported statements describing functions of genes from the GeneRIF Biological Term Annotations dataset. | |
| GeneSigDB Published Gene Signatures | PubMedIDs of publications reporting gene signatures containing MIR299 from the GeneSigDB Published Gene Signatures dataset. | |
| GEO Signatures of Differentially Expressed Genes for Gene Perturbations | gene perturbations changing expression of MIR299 gene from the GEO Signatures of Differentially Expressed Genes for Gene Perturbations dataset. | |
| GEO Signatures of Differentially Expressed Genes for Small Molecules | small molecule perturbations changing expression of MIR299 gene from the GEO Signatures of Differentially Expressed Genes for Small Molecules dataset. | |
| GEO Signatures of Differentially Expressed Genes for Transcription Factor Perturbations | transcription factor perturbations changing expression of MIR299 gene from the GEO Signatures of Differentially Expressed Genes for Transcription Factor Perturbations dataset. | |
| HuGE Navigator Gene-Phenotype Associations | phenotypes associated with MIR299 gene by text-mining GWAS publications from the HuGE Navigator Gene-Phenotype Associations dataset. | |
| JASPAR Predicted Transcription Factor Targets | transcription factors regulating expression of MIR299 gene predicted using known transcription factor binding site motifs from the JASPAR Predicted Transcription Factor Targets dataset. | |
| Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles | cell lines with high or low copy number of MIR299 gene relative to other cell lines from the Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles dataset. | |
| KnockTF Gene Expression Profiles with Transcription Factor Perturbations | transcription factor perturbations changing expression of MIR299 gene from the KnockTF Gene Expression Profiles with Transcription Factor Perturbations dataset. | |
| MotifMap Predicted Transcription Factor Targets | transcription factors regulating expression of MIR299 gene predicted using known transcription factor binding site motifs from the MotifMap Predicted Transcription Factor Targets dataset. | |
| Roadmap Epigenomics Histone Modification Site Profiles | histone modification site profiles with high histone modification abundance at MIR299 gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset. | |