| HGNC Family | Non-coding RNAs |
| Name | microRNA 520b |
| 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": "\nmiR‐520b plays a multifaceted role in modulating tumor cell migration and proliferation across several cancer types. In breast cancer, it functions as a suppressor of metastasis by directly targeting the 3′‐UTRs of genes such as HBXIP and interleukin‑8, thereby reducing aggressive cell migration (1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In hepatocellular carcinoma, restoration of miR‐520b levels leads to marked inhibition of tumor cell growth through the negative regulation of key oncogenic mediators including MEKK2, cyclin D1, and TET1 (2."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " This tumor‐suppressive trend is also observed in colorectal cancer, where miR‐520b downregulation correlates with enhanced malignant progression via deregulation of proteins like DCUN1D1 (9), and in head–neck cancers where miR‐520b represses epithelial–mesenchymal transition (EMT) and cancer stem cell traits by directly targeting CD44 (5). Additionally, in a broader context, the miR‐373/520 family, including miR‐520b/e, has been implicated in attenuating various oncogenic pathways (4).\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its effects on cell migration and proliferation, miR‐520b significantly contributes to the regulation of cancer stemness and chemotherapeutic responsiveness. In triple‐negative breast cancer, for instance, competitive endogenous RNA networks—such as those mediated by circIFI30—sequester miR‐520b, leading to increased CD44 expression and promoting tumor progression (6). In lung cancer, studies have demonstrated that miR‐520b can target molecules like HDAC4 and SPOP to modulate proliferation and activate downstream pathways such as Hedgehog signaling, although context‐dependent differences suggest that its role may vary between tumor types (7, 10."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Moreover, in breast cancer treated with doxorubicin, elevated miR‐520b facilitates apoptosis by attenuating the IGF‑1R/PI3K/AKT axis, thereby improving chemosensitivity (14).\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to direct tumor‐suppressive effects, miR‐520b is integrated into a complex regulatory network involving other non‐coding RNAs and stress‐responsive pathways. In prostate cancer, miR‐520b targets Capn4 to suppress Wnt/β‑catenin signaling (12), while in glioblastoma, its overexpression leads to a decrease in cyclin D1 levels and an increase in apoptosis, highlighting its importance in controlling cell cycle progression (13). Recent work also shows that under diverse cellular stress conditions, miR‐520b‑3p can directly bind to the 3′‑UTR of ATF5, reversing stress‐induced upregulation and promoting cell death (18). Furthermore, emerging evidence indicates that miR‐520b, along with closely related family members such as miR‑520e and miR‑520c, is subjected to regulation by long non‐coding RNAs—for example, Lnc‑ZFAS1 in osteosarcoma—to modulate downstream effectors like RHOC (19, 20). Collectively, these studies underscore the pivotal role of miR‑520b as a modulator of oncogenic and stress response pathways, offering promising targets for therapeutic intervention."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "1"}, {"type": "fg_fs", "start_ref": "6", "end_ref": "9"}, {"type": "fg_f", "ref": "2"}, {"type": "fg_fs", "start_ref": "10", "end_ref": "17"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_fs", "start_ref": "18", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Weiying Zhang, Zhanping Lu, Guangyao Kong, et al. 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| Synonyms | MIRN520B |
| NCBI Gene ID | 574473 |
| 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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MIR520B has 195 functional associations with biological entities spanning 4 categories (molecular profile, functional term, phrase or reference, cell line, cell type or tissue, gene, protein or microRNA) extracted from 10 datasets.
Click the + buttons to view associations for MIR520B 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 MIR520B 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 MIR520B 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 MIR520B 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 MIR520B gene from the ENCODE Transcription Factor Binding Site Profiles dataset. | |
| ENCODE Transcription Factor Targets | transcription factors binding the promoter of MIR520B gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset. | |
| GeneRIF Biological Term Annotations | biological terms co-occuring with MIR520B gene in literature-supported statements describing functions of genes from the GeneRIF Biological Term Annotations dataset. | |
| JASPAR Predicted Transcription Factor Targets | transcription factors regulating expression of MIR520B 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 MIR520B 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 MIR520B gene from the KnockTF Gene Expression Profiles with Transcription Factor Perturbations dataset. | |
| Roadmap Epigenomics Histone Modification Site Profiles | histone modification site profiles with high histone modification abundance at MIR520B gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset. | |