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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Tag]

ABSTRACT: The main goal of this study was to assess the role of LEF1 in patient-derived CLL cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE299962 | GEO | 2025/10/08

REPOSITORIES: GEO

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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [RNA-Seq]

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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Run]

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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Tag]

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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Run]

Project description:Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Run]

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Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [RNA-Seq]

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A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency

Project description:As a human tumor virus, EBV is present as a latent infection in its associated malignancies where genetic and epigenetic changes have been shown to impede cellular differentiation and viral reactivation. One such change is increased levels of the Wnt signaling effector, lymphoid enhancer binding factor 1 (LEF1) following EBV epithelial infection. In silico analysis of EBV type 1 and 2 genomes identified over 20 Wnt-response elements suggesting that LEF1 may directly bind the EBV genome and regulate the viral life cycle. Using CUT&RUN-seq, LEF1 was shown to bind the latent EBV genome at various sites encoding viral lytic products that included the immediate early transactivator BZLF1 and viral primase BSLF1 genes. SiRNA depletion of specific LEF1 isoforms revealed that the alternative-promoter derived isoform with an N-terminal truncation (∆N LEF1) transcriptionally repressed lytic genes associated with LEF1 binding. Furthermore, forced expression of the ∆N LEF1 isoform antagonized EBV reactivation from latency. The LEF1 mediated repression requires histone deacetylase activity through either recruitment or a direct intrinsic histone deacetylase activity. SiRNA depletion of LEF1 resulted in increased histone 3 lysine 9 and lysine 27 acetylation at LEF1 binding sites and across the EBV genome. These results support a novel role for LEF1 in maintaining EBV latency and restriction viral reactivation via repressive chromatin remodeling of critical lytic cycle factors

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LEF1 in Burkitt lymphoma

Project description:Recently global gene expression profiling of patients samples lead to a molecular definition of Burkitt Lymphoma (BL) with lymphocyte enhancer-binding factor 1 (LEF1) as a signature gene. Here we report the discovery of nucleic LEF1 in a very high proportion of BL cases (15/18) and LEF1 target genes. Germinal center B cells were devoid of detectable nuclear LEF1 expression as mantle cell lymphoma (0/5), marginal zone lymphoma (0/6), follicular lymphoma (0/12) or diffuse large B cell lymphoma (DLBCL) (1/31). Using whole genome gene expression profiling after transient knockdown of LEF1 in BL cell lines, new LEF1 target genes were identified. The joint expression of these genes in primary BL samples shows that LEF1 is not only expressed aberrantly in BL but also transcriptionally active. Our study identified aberrantly expressed LEF1 and its target genes suggesting an important functional role in BLs. 3 biological replicates scrb siRNA vs LEF1 si RNA , 4 siRNA are pooled

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LEF1 in Burkitt lymphoma

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The transcription factors TCF1 and LEF1 promote B-1a cell homeostasis and regulatory function

Project description:B-1 cells are innate-like immune cells found abundantly in serosal cavities and their secreted antibodies are enriched for bacterial recognition1–5. The subset known as “B-1a” repress inflammation by production of regulatory molecules including IL-10 6–8. Unlike conventional B cells, which are produced daily in the bone marrow, B-1a cells are primarily generated from foetal precursors and maintained through self-renewal 9. The mechanisms regulating B-1a homeostasis and function are incompletely understood. Here we demonstrate that serosal cavity mouse and human B-1 cells as well as chronic lymphocytic leukaemia (CLL) B cells express the transcription factors TCF1 and LEF1, and circulating TCF1+LEF1+ B-1 cells increase significantly in patients with bacterial pleural infection. LEF1 is expressed from foetal B-1 progenitors, while TCF1 expression is higher in peripheral B-1a cells. TCF1 and LEF1 deficiency significantly reduces B-1a cells in mice. These transcription factors support B-1a turn-over regulating Myc targets and metabolic pathways. Upon B-1 cell activation, TCF1/LEF1 induce formation of a stem-like population, partly through IL-10 production. TCF/LEF1-deficient B-1 cells proliferate excessively, acquire an exhausted/senescent phenotype, express reduced IL-10 and PD-L1, and fail to suppress brain inflammation. These findings reveal a transcriptional program that links stemness and regulatory potential in B-1a cells.

2025-08-14 | GSE294717 | GEO

The transcription factors TCF1 and LEF1 promote B-1a cell homeostasis and regulatory function.

Project description:B cells are innate-like immune cells found abundantly in serosal cavities and their secreted antibodies are enriched for bacterial recognition1–5. The subset known as “B-1a” repress inflammation by production of regulatory molecules including IL-10 6–8. Unlike conventional B cells, which are produced daily in the bone marrow, B-1a cells are primarily generated from foetal precursors and maintained through self-renewal 9. The mechanisms regulating B-1a homeostasis and function are incompletely understood. Here we demonstrate that serosal cavity mouse and human B-1 cells as well as chronic lymphocytic leukaemia (CLL) B cells express the transcription factors TCF1 and LEF1, and circulating TCF1+LEF1+ B-1 cells increase significantly in patients with bacterial pleural infection. LEF1 is expressed from foetal B-1 progenitors, while TCF1 expression is higher in peripheral B-1a cells. TCF1 and LEF1 deficiency significantly reduces B-1a cells in mice. These transcription factors support B-1a turn-over regulating Myc targets and metabolic pathways. Upon B-1 cell activation, TCF1/LEF1 induce formation of a stem-like population, partly through IL-10 production. TCF/LEF1-deficient B-1 cells proliferate excessively, acquire an exhausted/senescent phenotype, express reduced IL-10 and PD-L1, and fail to suppress brain inflammation. These findings reveal a transcriptional program that links stemness and regulatory potential in B-1a cells.

2025-08-14 | GSE298030 | GEO

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