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Beta globin locus transcript 3 (BGLT3)

Target
BGLT3
Molecular classification
Long non-coding RNA (lncRNA), Other
01

Overview

Beta globin locus transcript 3 (BGLT3) is a long non-coding RNA (lncRNA) located on chromosome 11p15.4 between the fetal (HBG1) and adult (HBD) globin genes, playing a regulatory role in the control of globin gene switching during erythropoiesis[1][3]. BGLT3 is also involved in cancer biology, notably acting as a tumor suppressor in chronic myeloid leukemia (CML) by antagonizing BCR-ABL-driven oncogenic pathways; its repression is necessary for BCR-ABL-mediated leukemic transformation, while restoration of BGLT3 expression is associated with increased apoptosis and CML cell death[1][3]. BGLT3 appears to function as a molecular sponge for oncogenic microRNAs (such as the miR-17~92 cluster and its paralogs miR-106a, miR-106b, miR-93, miR-20a, miR-20b), impacting critical pathways such as PI3K/AKT via PTEN regulation in cancer[1]. Therapeutically, BGLT3 is a candidate biomarker and target in CML, especially relevant in the setting of tyrosine kinase inhibitor resistance[1].\n\nBGLT3 has enhancer-like properties that support γ-globin (fetal globin) gene expression, making it of interest in hemoglobinopathies as well as leukemia[5]. The gene is also known by several aliases, including LINC01083, BGL3, and lncRNA-BGL3[2][3]. The relevance of BGLT3 in regulated erythroid gene expression and its role in cancer pathways suggests it is a functionally important and potentially actionable lncRNA[1][5].

Other names
LINC01083BGL3lncRNA-BGL3long intergenic non-protein coding RNA 1083beta globin locus 3CTD-2643I7.1
02

Mechanism of action

Indirect modulation: Restoring BGLT3 expression can promote apoptosis and suppress leukemia cell survival, particularly through miRNA pathway modulation and as part of the response to BCR-ABL kinase inhibitors[1].

03

Biological functions

Regulation of globin gene expressionEnhancer-like function for γ-globin activationTumor suppressor in myeloid cell contextModulation of miRNA sponge activity
04

Disease associations

Chronic myeloid leukemiaBeta-thalassemiaCancer (putative tumor suppressor in CML)
05

Safety considerations

Not established for therapeutic targeting of BGLT3; further functional and translational studies are required[1].
06

Interacting drugs

Tyrosine kinase inhibitors (indirect, e.g., imatinib, via BCR-ABL interaction and pathway regulation)
07

Biomarkers

Mutations in BGLT3 (e.g., NR_121648.1: n.203T>G, n.205T>A, n.432G>T in CML) may correlate with disease stage or treatment response in chronic myeloid leukemia[1].

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