BCL11A (BAF Chromatin Remodeling Complex Subunit BCL11A)

Our study elucidates a novel ceRNA network, the WT1-AS/miR-206/BCL11A axis, which regulates BC progression and modulates cuproptosis. These findings provide fresh insights into BC biology and highlight potential diagnostic and therapeutic targets centered on cuproptosis regulation.

Consequently, ectopic expression of BCL11A in LDB1-deficient proerythroblasts promotes their proliferation by rescuing them from ROS-mediated apoptosis. These findings highlight the essential role of LDB1 in fetal globin silencing during erythropoiesis.

The rescue experiments (overexpression of BCL11A combined with IFI6 or ferroptosis activator Erastin) were conducted to clarify the mechanism. Co-overexpression of IFI6 rescued the phenotype. This study reveals that BCL11A promotes ferroptosis by transcriptional inhibition of IFI6, thereby reducing TMZ resistance in glioma cells, providing a new strategy for combined targeting of IFI6 and ferroptosis.

Flow cytometry demonstrated that overexpression of BCL11A in vivo promoted intratumoral CD8+ T cell infiltration and activation, and increased PD-L1 expression. Our study confirmed BCL11A as a potential biomarker of clinical prognosis, immune infiltration, and neural-tumor interactions in PAAD, and might provide new insights for diagnosis and treatment of this tumor.

Using a battery of biophysical assays, we confirm that the BCL11A-CHD8 interaction is direct and identify chemical fragments that disrupt this interaction and affect downstream targets, decreasing proliferation in 3D colony assays. Our study provides a proof-of-principle approach for investigating tumour-specific protein-protein interactions and identifies lead chemical compounds that could be developed into novel therapeutics for TNBC.

A combined receiver operating characteristic (ROC) curve analysis revealed that the BCL11A-NTN5-OGN genes, which have specificity and sensitivity values of 0.968 and 0.901, respectively, can be used as a diagnostic biomarker for PRCC. In general, the genes introduced in this study may be used as diagnostic biomarkers for the early diagnosis of PRCC, thus providing the possibility of early treatment and preventing the progression of the disease.

miR-129-5p acts as a positive regulator of erythroid differentiation and γ-globin synthesis. It offers a promising miRNA target for activating the γ-globin gene and reducing ineffective erythropoiesis in β-thalassemia patients.

CD8RGs play an important role in regulating the TME of PAAD. Five hub genes-BCL11A, KLK11, GNG7, PHOSPHO1, and VCAM1-are closely associated with the prognosis of PAAD patients, providing new references for the exploration of biomarkers. Furthermore, our findings offer novel insights for clinical decision-making.

Despite a 60 % survival rate achieved with R-CHOP regiment for DLBCL, approximately 40 % of patients experience relapse or develop resistance to treatment...Furthermore, BCL11A protein expression levels demonstrated significant associations with P53 and C-MYC protein expression levels in the Germinal Center B-cell-like (GCB) subtype. These findings suggest that BCL11A may serve as a potential prognostic marker and therapeutic target for DLBCL.

Mechanistically, miR‑6747‑3p could specifically bind to the 546‑552 loci of BCL11A 3'‑UTR and induce γ‑globin expression. These data indicate that upregulation of miR‑6747‑3p affects red blood cell lineage development and induces HbF expression by targeting BCL11A in β‑thalassemia, highlighting miR‑6747‑3p as a potential molecular target for β‑thalassemia therapy.

Whole exome sequencing revealed loss of function mutations in TP53, STK11, PBRM1, SMAD3, FN1, NTRK1, and FANCD2, as well as gain of function mutations in MTOR, BCL11A and COL1A1, along with amplification of CCND3 and MDM2. This mutational landscape halfway between thymic carcinoma (TP53, PBRM1) and hepatoid variant carcinoma of other sites (STK11) suggests that, at some point during carcinogenesis, a switch occurred from an epithelial thymic phenotype to a hepatoid-like one.

Ectopic expression of a small peptide that contains the three zinc fingers can rescue the increase in 8-oxoguanine caused by BCL11A knockdown. These findings, together with previous results showing that BCL11A stimulates the enzymatic activities of NTHL1 and the Pol β polymerase, suggest that high expression of BCL11A is important to protect cancer cells against oxidative DNA damage.