A Bach2 Link between Pre-B Cell Receptor Checkpoint and Pre-B Cell ALL

Ye, B. Hilda; Mai, Yun

doi:10.1016/j.ccr.2013.08.017

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…BACH2, known as a B-cell tumor suppressor [19], plays a significant role in B-cell maturation, and the regulation of the pre-BCR checkpoint [20]. We have recognized that the balance between BACH2 and BCL6 can maintain the stringency of the GC B-cell repertoire [21], but the mechanism behind this competitive binding behavior by shared target promoters still needs to be investigated [20].…”

Section: Introductionmentioning

confidence: 99%

“…We have recognized that the balance between BACH2 and BCL6 can maintain the stringency of the GC B-cell repertoire [21], but the mechanism behind this competitive binding behavior by shared target promoters still needs to be investigated [20]. Recently, the oncogenic function of BACH2 has been utilized in several species of malignant tumor.…”

Section: Introductionmentioning

confidence: 99%

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MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

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The aim of the present study was to explore the mechanism through which miR-130a-3p affects the viability, proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC). Tissue samples were collected from the hospital department. NPC cell lines were purchased to conduct the in vitro and in vivo assays. A series of biological assays including MTT, Transwell, and wound healing assays were conducted to investigate the effects of miR-130a-3p and BACH2 on NPC cells. MiR-130a-3p was down-regulated in both NPC tissues and cell lines, whereas BACH2 was up-regulated in both tissues and cell lines. MiR-130a-3p overexpression inhibited NPC cell viability, proliferation, migration, and invasion but promoted cell apoptosis. The converse was true of BACH2, the down-regulation of which could inhibit the corresponding cell abilities and promote apoptosis of NPC cells. The target relationship between miR-130a-3p and BACH2 was confirmed. The epithelial–mesenchymal transition (EMT) pathway was also influenced by miR-130a-3p down-regulation. In conclusion, miR-130a-3p could bind to BACH2, inhibit NPC cell abilities, and promote cell apoptosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

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“…BCL6 orchestrates BACH2 protein stability in leukemia and lymphoma, and the BCL6/BACH2 axis equilibrium is crucial for controlling pre-BCR checkpoint cascades [ 124 ]. Furthermore, BACH2 is a transcriptional factor connected to the maturation of B-cell specificity and the establishment of germinal centers [ 125 , 126 , 127 ], and its transcription is activated by IKAROS. In pre-B-ALL, chronic myeloid leukemia, and Ph-positive ALL cells, it performs as a tumor suppressor, controls the pre-BCR checkpoint and promotes apoptosis in response to oxidative stress [ 128 , 129 , 130 ].…”

Section: Loss Of Function Of Ikaros In All: What’s Up?mentioning

confidence: 99%

IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?

Conserva

Redavid

Anelli

et al. 2023

IJMS

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One key process that controls leukemogenesis is the regulation of oncogenic gene expression by transcription factors acting as tumor suppressors. Understanding this intricate mechanism is crucial to elucidating leukemia pathophysiology and discovering new targeted treatments. In this review, we make a brief overview of the physiological role of IKAROS and the molecular pathway that contributes to acute leukemia pathogenesis through IKZF1 gene lesions. IKAROS is a zinc finger transcription factor of the Krüppel family that acts as the main character during hematopoiesis and leukemogenesis. It can activate or repress tumor suppressors or oncogenes, regulating the survival and proliferation of leukemic cells. More than 70% of Ph+ and Ph-like cases of acute lymphoblastic leukemia exhibit IKZF1 gene variants, which are linked to worse treatment outcomes in both childhood and adult B-cell precursor acute lymphoblastic leukemia. In the last few years, much evidence supporting IKAROS involvement in myeloid differentiation has been reported, suggesting that loss of IKZF1 might also be a determinant of oncogenesis in acute myeloid leukemia. Considering the complicated “social” network that IKAROS manages in hematopoietic cells, we aim to focus on its involvement and the numerous alterations of molecular pathways it can support in acute leukemias.

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“…BTB and CNC Homology 1 Basic Leucine Zipper Transcription Factor 2 (BACH2) is a transcriptional factor associated with the germinal center formation and affinity maturation of B-cells [87][88][89][90]. It functions as a tumor suppressor and pre B-cell receptor checkpoint in pre B-ALL, CML, and Ph-positive ALL cells and induces apoptosis in response to oxidative stress [91][92][93].…”

Section: B-cell Lymphoma 6 (Bcl6) and Btb And Cnc Homology 1 Basic Lementioning

confidence: 99%

Transcriptional Regulation of Genes by Ikaros Tumor Suppressor in Acute Lymphoblastic Leukemia

Dhanyamraju

Iyer

Smink

et al. 2020

IJMS

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Regulation of oncogenic gene expression by transcription factors that function as tumor suppressors is one of the major mechanisms that regulate leukemogenesis. Understanding this complex process is essential for explaining the pathogenesis of leukemia as well as developing targeted therapies. Here, we provide an overview of the role of Ikaros tumor suppressor and its role in regulation of gene transcription in acute leukemia. Ikaros (IKZF1) is a DNA-binding protein that functions as a master regulator of hematopoiesis and the immune system, as well as a tumor suppressor in acute lymphoblastic leukemia (ALL). Genetic alteration or functional inactivation of Ikaros results in the development of high-risk leukemia. Ikaros binds to the specific consensus binding motif at upstream regulatory elements of its target genes, recruits chromatin-remodeling complexes and activates or represses transcription via chromatin remodeling. Over the last twenty years, a large number of Ikaros target genes have been identified, and the role of Ikaros in the regulation of their expression provided insight into the mechanisms of Ikaros tumor suppressor function in leukemia. Here we summarize the role of Ikaros in the regulation of the expression of the genes whose function is critical for cellular proliferation, development, and progression of acute lymphoblastic leukemia.

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A Bach2 Link between Pre-B Cell Receptor Checkpoint and Pre-B Cell ALL

Abstract: Bach2 is a transcription factor required for affinity maturation of B cells. A recent study reveals, quite unexpectedly, that Bach2 also plays a key role in the pre-B cell receptor checkpoint and functions as a tumor suppressor in pre-B cell acute lymphocytic leukemia.

Cited by 5 publications

References 10 publications

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?

Transcriptional Regulation of Genes by Ikaros Tumor Suppressor in Acute Lymphoblastic Leukemia

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