MIR205 host gene (MIR205HG)

MIR205 host gene (MIR205HG) is a long non-coding RNA located on human chromosome 1q32.2, comprised of 4–5 exons and varying splice forms, typically around 940–5900 bp in length[1][2]. MIR205HG acts as a regulatory lncRNA, most notably serving as the host for miR-205 microRNAs (miR-205-5p and miR-205-3p)[2][3]. It exerts complex functions in cancer biology: in head and neck squamous cell carcinoma (HNSCC), it is overexpressed in mutant TP53 contexts, driving proliferation, migration, and oncogenic activity, likely through modulation of cyclin genes and cell cycle control[1]. In esophageal adenocarcinoma (EAC) and Barrett’s esophagus (BE), MIR205HG is downregulated and functions as a tumor suppressor, inhibiting cell proliferation, colony formation, and invasion, partly by suppressing the Hedgehog signaling pathway[2]. Its longitudinal expression in tissues such as cervix, prostate, trachea, and thymus suggests broader regulatory significance[2]. While not presently a therapeutic target, its dysregulation is implicated in cancer progression and may be leveraged as a biomarker. For future structured data extraction, this entry summarizes: MIR205HG is a long non-coding RNA acting as a host gene for miR-205, with mixed pro-oncogenic and tumor suppressor roles, contextually dependent on cancer type and genetic background[1][2].

Other names

LINC00510LEADR (Long Epithelial Alu-interacting Differentiation-related RNA)miPEP205NPC-A-5NONHSAG004163.1Long intergenic non-protein coding RNA 510Long Epithelial Alu-interacting Differentiation-related RNAMIR205HG (non-protein coding)

No drugs currently target MIR205HG directly. Its biological influence (e.g., modulation of proliferation, migration, and cell cycle) is due to its endogenous functions, not therapeutic intervention[1][2].