Knockdown of Bcl-3 Inhibits Cell Growth and Induces DNA Damage in HTLV-1-infected Cells)

Gao, Cai; Wang, Xia; Chen, Lin; Wang, Jin-Heng; Zhi, Gao; Wang, Hui

doi:10.7314/apjcp.2013.14.1.405

Cited by 4 publications

(4 citation statements)

References 25 publications

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“…Early indications of a role for BCL3 in genome integrity were posited when BCL3 was shown to suppress p53 via upregulation of Hdm2 in response to UVB induced DNA damage of breast cancer cells [ 105 ] and when shRNA suppression of BCL3 was shown to induce aneuploidy in HeLa cells with accompanying increases in phospho-ATM, gamma-H2Ax and a concomitant decrease in phospho-CHK1 [ 114 ]. These observations were further supported by studies demonstrating a relative loss of DNA integrity when BCL3 was suppressed following human T cell leukemia virus Type 1 (HTLV1) challenge in T-cells [ 115 ] and a role in DNA break repair proposed after profound suppression of the double-strand DNA break repair protein DNA-PK in HeLa cells was observed when BCL3 was suppressed both before and after UVB irradiation [ 110 ].…”

Section: Bcl3 and Cancermentioning

confidence: 81%

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Seaton,

Smith,

Brancale

et al. 2024

Mol Cancer

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In the early 1990’s a group of unrelated genes were identified from the sites of recurring translocations in B-cell lymphomas. Despite sharing the nomenclature ‘Bcl’, and an association with blood-borne cancer, these genes have unrelated functions. Of these genes, BCL2 is best known as a key cancer target involved in the regulation of caspases and other cell viability mechanisms. BCL3 on the other hand was originally identified as a non-canonical regulator of NF-kB transcription factor pathways – a signaling mechanism associated with important cell outcomes including many of the hallmarks of cancer. Most of the early investigations into BCL3 function have since focused on its role in NF-kB mediated cell proliferation, inflammation/immunity and cancer. However, recent evidence is coming to light that this protein directly interacts with and modulates a number of other signaling pathways including DNA damage repair, WNT/β-catenin, AKT, TGFβ/SMAD3 and STAT3 – all of which have key roles in cancer development, metastatic progression and treatment of solid tumours. Here we review the direct evidence demonstrating BCL3’s central role in a transcriptional network of signaling pathways that modulate cancer biology and treatment response in a range of solid tumour types and propose common mechanisms of action of BCL3 which may be exploited in the future to target its oncogenic effects for patient benefit.

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Section: Bcl3 and Cancermentioning

confidence: 81%

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Seaton,

Smith,

Brancale

et al. 2024

Mol Cancer

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“…In studying the specific role of Bcl-3 in cells infected with human T cell leukemia virus type 1 (HTLV-1), Gao et al used shRNA to knock down the expression of Bcl-3. The experimental results revealed that Bcl-3 can promote DNA stability, cell growth and NF-kB activation in HTLV-1-infected cells (66). Moreover, Bcl-3 mutations in lymphocytes give rise to overexpression of IkB protein and uncontrolled cell proliferation, which lead to B-cell chronic lymphocytic leukemia (67).…”

Section: Bcl-3 Is Involved In Cell Survival and Apoptosismentioning

confidence: 99%

Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation

et al. 2022

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The NF-κB transcription factor family controls the transcription of many genes and regulates a number of pivotal biological processes. Its activity is regulated by the IκB family of proteins. Bcl-3 is an atypical member of the IκB protein family that regulates the activity of nuclear factor NF-κB. It can promote or inhibit the expression of NF-κB target genes according to the received cell type and stimulation, impacting various cell functions, such as proliferation and differentiation, induction of apoptosis and immune response. Bcl-3 is also regarded as an environment-dependent cell response regulator that has dual roles in the development of B cells and the differentiation, survival and proliferation of Th cells. Moreover, it also showed a contradictory role in inflammation. At present, in addition to the work aimed at studying the molecular mechanism of Bcl-3, an increasing number of studies have focused on the effects of Bcl-3 on inflammation, immunity and malignant tumors in vivo. In this review, we focus on the latest progress of Bcl-3 in the regulation of the NF-κB pathway and its extensive physiological role in inflammation and immune cells, which may help to provide new ideas and targets for the early diagnosis or targeted treatment of various inflammatory diseases, immunodeficiency diseases and malignant tumors.

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“…Cloning of chromosomal breakpoints found in chronic lymphocytic leukemia cells demonstrated that the t(14;19) chromosomal translocation results in the juxtaposition of the BCL3 gene with the immunoglobulin (Ig) heavy locus leading to the overexpression of Bcl-3 in leukemic cells [ 19 , 20 , 21 ]. Bcl-3 overexpression is also associated with a number of cancers that do not harbor BCL3 -associated translocations, including classical Hodgkin’s and peripheral T-cell lymphoma [ 22 ], chronic lymphocytic leukemia [ 23 ], adult T cell leukemia [ 24 ], and certain solid tumors [ 25 , 26 ].…”

Section: Bcl-3mentioning

confidence: 99%

Regulation of the Adaptive Immune Response by the IκB Family Protein Bcl-3

Herrington

Nibbs

2016

Cells

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Bcl-3 is a member of the IκB family of proteins and an important regulator of Nuclear Factor (NF)-κB activity. The ability of Bcl-3 to bind and regulate specific NF-κB dimers has been studied in great depth, but its physiological roles in vivo are still not fully understood. It is, however, becoming clear that Bcl-3 is essential for the proper development, survival and activity of adaptive immune cells. Bcl-3 dysregulation can be observed in a number of autoimmune pathologies, and Bcl3-deficient animals are more susceptible to bacterial and parasitic infection. This review will describe our current understanding of the roles played by Bcl-3 in the development and regulation of the adaptive immune response, including lymphoid organogenesis, immune tolerance, lymphocyte function and dendritic cell biology.

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Knockdown of Bcl-3 Inhibits Cell Growth and Induces DNA Damage in HTLV-1-infected Cells)

Cited by 4 publications

References 25 publications

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation

Regulation of the Adaptive Immune Response by the IκB Family Protein Bcl-3

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