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Table 1 Relationship of HOTAIR with other non-coding RNAs and proteins

From: The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

miR IDStatusFunctionDiseaseReference
miR-148aUpstreammiR-148 activity represses HOTAIR expression by interacting with the corresponding promoter regionBreast cancer[73]
miR-1UpstreammiR-1 supresses expression of HOTAIR and MAPK1 activity, prohibiting cell proliferation, invasion and migrationOvarian cancer[63]
miR-214-3pUpstreammiR-214-3p supresses expression of HOTAIR and MAPK1 activityOvarian cancer[63]
miR-330-5pUpstreammiR-330-5p supresses expression of HOTAIR and MAPK1 activityOvarian cancer[63]
miR-206CompetingUp-regulates BCL-W by sponging miR-206, elevating cell proliferation rateBreast cancer[62]
miR-130aCompetingHOTAIR represses miR-130a, likely in a reciprocal negative feedback loop, competition in binding to similar RISC complexGalbladder cancer[65]
miR-34aDownstreamHOTAIR epigenetically supresses miR-34a, leading to up-regulation of SOX2 and cell proliferationBreast cancer[64]
miR-7DownstreamHOTAIR supresses expression of HOXD10 and subsequent target, miR-7, ultimately promoting EMT process due to up-regulation of SETDB1 and STAT3Breast cancer[78]
miR-20a-5pDownstreamHOTAIR promotes cell growth, mobility and invasiveness via supressing miR-20a-5p and consequently up-regulating HMGA2Breast cancer[83]
miR-218DownstreamHOTAIR induces radioresistance by reducing miR-218 expression level and apoptosisBreast cancer[102]
miR-138/204/217DownstreamHOTAIR directly antagonizes this complex, ultimately overexpressing EZH2 as a target of miR-138/217Renal cell carcinoma[84]
miR-200cDownstreamHOTAIR promotes epigenetic silencing of miR-200c, Through PRC2-EZH2 complexRenal cell carcinoma[84]
miR-141DownstreamHOTAIR epigenetically inhibits miR-141 expressionGlioma[56]
miR-326DownstreamInhibit miR-326 activityGlioma[57]