| HGNC Family | Non-coding RNAs |
| Name | microRNA 6844 |
| 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": "\nSeveral studies have characterized the functions of synaptic adhesion molecules of the SALM/Lrfn family in neural development. One investigation demonstrated that all five SALM proteins promote neurite outgrowth in cultured hippocampal neurons with distinct phenotypic outcomes, emphasizing the importance of both the N-terminal extracellular regions and the C-terminal PDZ binding domains in mediating these effects (for example, directing neurite extension) ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "]. In complementary work, SALM4 was found to act as a negative regulator of excitatory synapse development by cis-inhibiting SALM3’s synaptogenic function, a mechanism that is further underscored by behavioral and electrophysiological changes in knockout mice ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "].\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast to the neural context described above, miR-6844 has been investigated specifically in breast cancer cells. This microRNA plays a pivotal role in sustaining the stemness and self‐renewal properties of breast cancer stem-like cells. Downregulation of miR-6844 in mammosphere cultures derived from MCF-7 and T47D cells significantly reduces cell proliferation and sphere formation, concomitantly decreasing key stemness markers such as Bmi-1, Nanog, c-Myc, Sox2, and CD44. Mechanistically, the loss of miR-6844 disrupts the CD44‐JAK2-STAT3 signaling axis—an effect evidenced by diminished phosphorylation of JAK2 and STAT3, downregulation of cell cycle regulators CCND1 and CDK4 leading to G2/M arrest, and the induction of apoptotic pathways along with reduced migratory and invasive behavior ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "].\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Philip Y Wang, Gail K Seabold, Robert J Wenthold "}, {"type": "b", "children": [{"type": "t", "text": "Synaptic adhesion-like molecules (SALMs) promote neurite outgrowth."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cell Neurosci (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.mcn.2008.05.019"}], "href": "https://doi.org/10.1016/j.mcn.2008.05.019"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18585462"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18585462"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Eunkyung Lie, Ji Seung Ko, Su-Yeon Choi, et al. "}, {"type": "b", "children": [{"type": "t", "text": "SALM4 suppresses excitatory synapse development by cis-inhibiting trans-synaptic SALM3-LAR adhesion."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Commun (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ncomms12328"}], "href": "https://doi.org/10.1038/ncomms12328"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27480238"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27480238"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Eunkyung Lie, Yeji Yeo, Eun-Jae Lee, et al. "}, {"type": "b", "children": [{"type": "t", "text": "SALM4 negatively regulates NMDA receptor function and fear memory consolidation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Commun Biol (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s42003-021-02656-3"}], "href": "https://doi.org/10.1038/s42003-021-02656-3"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34588597"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34588597"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Kumari Sunita Prajapati, Shashank Kumar "}, {"type": "b", "children": [{"type": "t", "text": "Loss of miR-6844 alters stemness/self-renewal and cancer hallmark(s) markers through CD44-JAK2-STAT3 signaling axis in breast cancer stem-like cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Biochem (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/jcb.30441"}], "href": "https://doi.org/10.1002/jcb.30441"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "37436061"}], "href": "https://pubmed.ncbi.nlm.nih.gov/37436061"}]}]}]}
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| Synonyms | HSA-MIR-6844 |
| NCBI Gene ID | 102466200 |
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| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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MIR6844 has 0 functional associations with biological entities spanning 0 categories () extracted from 0 datasets.
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If available, associations are ranked by standardized value
| Dataset | Summary |
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