MIR155 host gene (MIR155HG)

MIR155 host gene (MIR155HG), also known as B-cell integration cluster (BIC), is a long non-coding RNA gene that acts as the primary transcript (host gene) for microRNA-155 (miR-155)[1][2][3]. MIR155HG is transcribed as a capped, polyadenylated, multi-exonic RNA that does not code for proteins, but is processed to produce miR-155, a well-characterized regulator of hematopoiesis, inflammation, cancer, and antiviral immunity[1][4]. The lncRNA form itself also has independent roles, including modulation of antigen presentation (via HSPA8), IFN-β production, and serving as a competitive endogenous RNA sponge for other miRNAs[3][4]. MIR155HG and its processed products are overexpressed in multiple malignancies, promote proliferation and chemoresistance, and modulate STAT3/NF-κB signaling; they have roles in immune response, inflammation, and serve as promising biomarkers and targets for therapeutic intervention, though direct clinical inhibition remains experimental[2][4].

Other names

B-cell integration clusterBICBIC-155miPEP155P155microRNA host gene 2lncRNA-155NCRNA00172LncRNA-SERBB-cell receptor inducible, non-protein coding RNA 172LncRNA with specific ER beta bindingMIRHG2

Drugs and experimental compounds targeting MIR155HG or miR-155 act by inhibiting its expression or blocking its function, leading to altered cell survival, proliferation, and immune modulation[2][1]. MIR155HG overexpression confers chemoresistance (reduces apoptosis in response to chemotherapeutics). Some immunity-related mechanisms involve modulation of IFN-β via the lncRNA and STAT1 via miR-155-5p[4].