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BTG1 is a member of the TOB/BTG protein family, which is a transducer of ErbB-2 and TOB2. All members of TOB/BTG protein family can inhibit cell proliferation and cell cycle progression, stimulating cellular differentiation.
BTG proteins can shuttle in nucleocytoplasmic counterparts because of their nuclear localization and export signals. There is the highest BTG1 expression in G0/G1 phases and is down-regulated as the cells cycle progresses in G1 phase. Further investigation shows that BTG1 protein can bind to nuclear receptor TRα and the myogenic factor MyoD, protein arginine methyltransferase 1, and human carbon catabolite repressor protein-associative factor 1. BTG1 overexpression is detectable in apoptotic cells and helpful for anti-sense Bcl-2-induced cytotoxic effects.
Low Expression of BTG1 in Pancreatic Ductal Adenocarcinoma is Associated with Prognosis
BTG1 expression is barely detectable in brain and muscle tissues which are fully differentiated, but can be detected in cells, which can still respond to various signals, especially in G0/G1 transition. The expression of BTG1 is the highest in the G0/G1 phases of the cell cycle and is decreased when cells progress through G1, so BTG1 overexpression can inhibit cell proliferation and cell cycle progression, increase cell apoptosis, and decrease the expression of vascular endothelial growth factor in tumors. Recent studies have shown that BTG1 expression levels are significantly lower in PDAC tissues than in normal adjacent non-cancerous tissues, which suggests that BTG1 expression may serve as an available prognostic biomarker and a novel molecular in the future.
BTG1 Expression Correlates with Pathogenesis, Aggressive Behaviors of cervical cancer and ovarian cancer
BTG1 was reported to enhance Hoxb9 (homeodomain protein)-induced transcription to suppress proliferation in HeLa cells, Prévôt et al. has reported that BTG1 enhance Hoxb9-mediated transcription in transfected cells, and the formation of a Hoxb9-BTG1 complex on a Hoxb9-responsive target, and the fact that this interaction facilitates the binding of Hoxb9 to DNA. Another study found that BTG1 overexpression suppressed proliferation, migration and invasion, and induced chemo-sensitivity to cisplatin, G1 arrest and apoptosis of ovarian cancer cells. BTG1 mRNA expression in International Federation of Gynecology and Obstetrics (FIGO) stage I/II ovarian carcinomas was higher than that in FIGO III/IV ovarian carcinomas. In BTG1-silenced ovarian cancer cells, the BTG1 promoter was highly methylated. Altered BTG1 expression might play a role in the pathogenesis and progression of ovarian carcinoma by modulating proliferation, migration, invasion, cell cycle, and apoptosis.
Tumor Suppressor BTG1 Limits the Activation of BCL6 Expression
B cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most common malignancy in children and is characterized by the presence of distinct genetic abnormalities. The t (12; 21) (p13; q22) chromosomal translocation occurs in utero, giving rise to the ETV6-RUNX1 fusion protein and generating a preleukemic clone, but additional cooperative events are required before the onset of overt leukemia. Several studies have reported that monoallelic BTG1 deletions in ETV6-RUNX1-positive BCP-ALL are the result of genomic rearrangements mediated by aberrant RAG recombinase activity. BTG1 functions as a transcriptional cofactor that acts by recruiting effector molecules, such as protein arginine methyltransferase I (PRMT1), to specific transcription factors, thus affecting proliferation and differentiation.
BCL6 has been identified as a critical determinant of leukemic stem cell survival in chronic myeloid leukemia, involving repression of TP53. Recent study has indicated that BCL6 promotes proliferation of primitive B-lymphoid progenitors by suppressing the p53 pathway. Esther et al. revealed that downstream targets of BCL6 including p19Arf and Tp53, are down-regulated in ETV6-RUNX1-positive fetal progenitor B cells, particularly in the absence of BTG1 function.