An investigation of methylation pattern changes in the IKZF1 promoter in patients with childhood B-cell acute lymphoblastic leukemia

Rahmani, Mina; Fardi, Masoumeh; Hagh, Majid Farshdousti; Feizi, Abbas Ali Hosseinpour; Talebi, Mehdi; Solali, Saeed

doi:10.5045/br.2019.54.2.144

Cited by 4 publications

(3 citation statements)

References 24 publications

(29 reference statements)

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“…A recent study by Rahmani et al suggested that, in B-ALL patients, overexpression of IKZF1 may contribute to B-cell differentiation arrest and proliferation induction. Therefore, when investigating the methylation status of CpG islands in the promoter region of IKZF1 in B-ALL cells of children, a hypomethylation pattern of the gene promoter was observed in 96% of B-ALL samples [ 97 ].…”

Section: Ikzf1 Dysregulation In All: a Mean “Hater”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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Section: Ikzf1 Dysregulation In All: a Mean “Hater”mentioning

confidence: 99%

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

Conserva

Redavid

Anelli

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Ikaros activities are thought to be regulated by post-translational phosphorylation, small ubiquitin-related modifier (SUMOylation), and ubiquitination ( Sridharan and Smale, 2007 ). Besides, the hypomethylated pattern of CpG island in the IKZF1 promoter region may be the basis of abnormal Ikaros expression patterns associated with malignant tumors ( Chen et al, 2019 ; Rahmani et al, 2019 ). SUMOylation interferes in the interaction of Ikaros with transcriptional co-repressors SIN3A, SIN3B, Mi-2β, and CtBP and weakens the inhibitory activity of Ikaros ( Gómez-del Arco et al, 2005 ).…”

Section: Ikaros Family Signalingmentioning

confidence: 99%

Ikaros Proteins in Tumor: Current Perspectives and New Developments

Xia

Yuan

Han

et al. 2021

Front. Mol. Biosci.

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Ikaros is a zinc finger transcription factor (TF) of the Krüppel family member, which significantly regulates normal lymphopoiesis and tumorigenesis. Ikaros can directly initiate or suppress tumor suppressors or oncogenes, consequently regulating the survival and proliferation of cancer cells. Over recent decades, a series of studies have been devoted to exploring and clarifying the relationship between Ikaros and associated tumors. Therapeutic strategies targeting Ikaros have shown promising therapeutic effects in both pre-clinical and clinical trials. Nevertheless, the increasingly prominent problem of drug resistance targeted to Ikaros and its analog is gradually appearing in our field of vision. This article reviews the role of Ikaros in tumorigenesis, the mechanism of drug resistance, the progress of targeting Ikaros in both pre-clinical and clinical trials, and the potential use of associated therapy in cancer therapy.

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“…Childhood acute leukemia (AL) is the most common malignant tumor that invades the blood system of children. It is also the malignant tumor of children with the highest incidence rate, which seriously threatens the life and health of children (1)(2)(3). At present, the pathogenesis of childhood AL remains unclear.…”

Section: Introductionmentioning

confidence: 99%

GEM on proliferation and apoptosis of childhood AL cells through inhibiting c‑myc expression by upregulating miR‑125a‑3p

Xing

Yin

et al. 2020

Oncol Lett

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Effect of gemcitabine (GEM) on proliferation and apoptosis of childhood acute leukemia (AL) cells and the mechanism of action were investigated. Bone marrow and peripheral blood of 18 newly diagnosed children with childhood AL admitted to Yidu Central Hospital of Weifang were selected, and the miR-125a-3p level in peripheral blood of healthy children and children with AL was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Leukemia cells from the bone marrow of children with AL were primarily cultured and purified to observe the morphology. miR-125a-3p mimic was transfected into childhood AL cells. The cells were randomly divided into three groups: control group, GEM group and GEM + miR-125a-3p mimic group. 5-ethynyl-2'-deoxyuridine (EdU) staining assay was chosen to detect the proliferation of childhood AL cells in each group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining assay was adopted to determine apoptosis of childhood AL cells. The protein level of c-myc was measured via western blotting. Compared with that in the healthy children, the level of miR-125a-3p in the peripheral blood of children with AL was remarkably decreased. Compared with those in the control group, GEM inhibited proliferation and promoted apoptosis of childhood AL cells, and impeded the protein expression of c-myc in these cells. Compared with those in the GEM group, GEM + miR-125a-3p mimic notably reduced the proliferation and enhanced apoptosis of cells, and the protein expression of c-myc in cells was overtly reduced. The level of miR-125a-3p in peripheral blood of children with AL is obviously decreased. It is suggested in this study that GEM can inhibit the proliferation and promote apoptosis of childhood AL cells, and the mechanism may be related to upregulated miR-125a-3p inhibiting the expression of c-myc.

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An investigation of methylation pattern changes in the IKZF1 promoter in patients with childhood B-cell acute lymphoblastic leukemia

Cited by 4 publications

References 24 publications

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

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

Ikaros Proteins in Tumor: Current Perspectives and New Developments

GEM on proliferation and apoptosis of childhood AL cells through inhibiting c‑myc expression by upregulating miR‑125a‑3p

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