BCL3

Last update 08 May 2025

Basic Info

Synonyms

B-cell lymphoma 3 protein, BCL-3, BCL3

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Introduction

Contributes to the regulation of transcriptional activation of NF-kappa-B target genes. In the cytoplasm, inhibits the nuclear translocation of the NF-kappa-B p50 subunit. In the nucleus, acts as transcriptional activator that promotes transcription of NF-kappa-B target genes. Contributes to the regulation of cell proliferation (By similarity).

100 Clinical Results associated with BCL3

100 Translational Medicine associated with BCL3

0 Patents (Medical) associated with BCL3

682

Literatures (Medical) associated with BCL3

01 Apr 2025·Journal of Biological Chemistry

Immune checkpoint protein PD-L1 promotes transcription of angiogenic and oncogenic proteins IL-8, Bcl3, and STAT1 in ovarian cancer cells

Article

Author: Reddy, Suprataptha U ; Vancura, Ales ; Gaire, Bijaya ; Sham, Rachel ; Smith, Khalani ; Vancurova, Ivana

Immunotherapies blocking cell surface signaling of the immune checkpoint PD-L1 have shown great promise in several cancers, but the results have been disappointing in ovarian cancer (OC). One of the main underlying mechanisms likely consists of the cell-intrinsic intracellular functions of PD-L1, which are incompletely understood. The expression of PD-L1 in OC cells is induced by interferon-γ (IFNγ), a pleiotropic cytokine produced in response to chemotherapy or immune checkpoint blockade. We have recently shown that IFNγ induces expression of the proto-oncogene Bcl3, the proangiogenic chemokine interleukin-8 (IL-8)-CXCL8, and the transcription factor STAT1, resulting in increased OC cell proliferation and migration. Here, we report that IFNγ-induced expression of PD-L1 results in PD-L1 recruitment to IL-8, Bcl3, and STAT1 promoters. The occupancy of PD-L1 at IL-8, Bcl3, and STAT1 promoters is associated with increased histone acetylation and RNA polymerase II recruitment to these promoters. Suppression of IFNγ-induced PD-L1 decreases the expression of IL-8, Bcl3, and PD-L1 and increases apoptosis in OC cells. Together, these findings demonstrate that PD-L1 promotes transcription of IL-8, Bcl3, and STAT1, thus providing a novel function of PD-L1 in cancer cells, and suggesting that the increased IL-8, Bcl3, and STAT1 expression mediated by PD-L1 might contribute to the limited effectiveness of cancer immunotherapies targeting the surface expression of PD-L1 in OC.

01 Jan 2025·International Journal of Experimental Pathology

Identification of BCL3 as a biomarker for chondrocyte programmed cell death in osteoarthritis

Article

Author: Xu, Yongqing ; Ren, Junxiao ; Meng, Chen ; Li, Rui ; Li, Chuan

AbstractOsteoarthritis (OA) is a condition that is widely prevalent and causes joint pain and disability, with programmed cell death (PCD) playing a role in its pathogenesis. This study aimed to identify biomarkers associated with PCD in OA and explore their potential roles. Three RNA‐sequencing datasets (GSE114007, GSE51588 and GSE220243) related to OA were analysed. Differential expression and weighted gene co‐expression network identified key differentially expressed PCD‐related genes (DE‐PRMGs). Potential biomarkers were identified and validated through receiver operating characteristic (ROC) curves, correlation analyses, gene set enrichment analysis, single‐cell expression and RT‐qPCR. A total of 45 DE‐PRMGs were identified, affecting pathways like TNF signalling and RNA degradation. BCL3, TREM2 and NRP2 were prioritized as potential OA biomarkers, which are associated with ribosome function and immune cell infiltration and potentially linked to PCD. The functional role of one of the molecules identified, BCL3, was explored further using a cell model of inflammation induced chondrocytes. BCL3 was significantly down regulated in OA samples from the public dataset and clinical samples analysed by RT‐qPCR. BCL3 overexpression reduced apoptosis in chondrocytes stimulated with inflammatory cytokines. Thus the functional studies highlighted the anti‐apoptotic role of BCL3 in chondrocytes and provide new insights into OA pathogenesis with potential for future therapeutic development.

01 Jan 2025·Cellular and Molecular Gastroenterology and Hepatology

Liver-specific Bcl3 Knockout Alleviates Acetaminophen-induced Liver Injury by Activating Nrf2 Pathway in Male Mice

Article

Author: Gao, Jingtao ; Gao, Ge ; Kang, Xue ; Lv, Yang ; Lu, Wei ; Ma, Haowen ; Jiang, Shan ; Xin, Yue ; Liang, Yinming ; Sheng, Xiaohang ; Zhao, Yuxin ; Wang, Hui ; Niu, Yuna

BACKGROUND & AIMSAcetaminophen (APAP) overdose is the leading cause of acute liver failure, with oxidative stress being a critical factor in this process. Glutathione (GSH) plays a vital defensive role. Activation of nuclear factor erythroid 2 like 2 (Nrf2) pathway mitigates APAP-induced liver damage by promoting GSH biosynthesis and enhancing drug detoxification. Although the role of B cell leukemia/lymphoma 3 (Bcl3) in regulating inflammatory responses, cellular oncogenesis, and immune balance is well-documented, its function in APAP-induced liver injury remains unclear.METHODSWe employed liver-specific Bcl3 knockout (Bcl3^hep-/-) mice and adeno-associated virus (AAV)-8-mediated Bcl3 overexpression (AAV-Bcl3) mice to model APAP-induced liver injury. Liver damage was assessed through hematoxylin and eosin staining and serum alanine aminotransferase and aspartate aminotransferase measurements. The interaction between Bcl3 and Nrf2 was examined using immunofluorescence and co-immunoprecipitation assays.RESULTSOur study reveals a significant upregulation of Bcl3 expression in the livers of male mice following APAP administration, suggesting Bcl3's potential involvement in this pathological process. In Bcl3^hep-/- mice, a reduced severity of liver damage was observed at both 6 and 24 hours post-APAP treatment compared with controls. Notably, Bcl3-deficient mice exhibited accelerated GSH replenishment due to the rapid induction of Gclc and Gclm genes following 6 hours of APAP exposure. Through immunofluorescence and co-immunoprecipitation analyses, we identified an interaction between Bcl3 and Nrf2. The loss of Bcl3 enhanced Nrf2 translocation upon APAP challenge, leading to the upregulation of antioxidant gene expression. These findings suggest that Bcl3 knockout alleviates oxidative stress resulting from APAP overdose.CONCLUSIONWe uncovered a previously uncharacterized role of Bcl3 in APAP-induced liver injury, emphasizing the role of the Bcl3-Nrf2 axis in oxidative stress-related liver damage.

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BCL3

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