Crosstalk between hnRNP K and SET in ATRA‐induced differentiation in acute promyelocytic leukemia

Padovani, Karina Stringhetta; Goto, Renata Nishida; Fugio, Lais Brigliadori; Garcia, Cristiana Bernadelli; Alves, Vâni Maria; Brassesco, María Sol; Greene, Lewis Joel; Rego, Eduardo Magalhães; Leopoldino, Andréia Machado

doi:10.1002/2211-5463.13210

Cited by 4 publications

(2 citation statements)

References 49 publications

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“…However, hnRNP K might be an oncogene due to its significant overexpression in the bone marrow of non-remission AML patients and drug-resistant cell lines ( 89 , 90 ). hnRNP K expression was positively correlated with that of autophagy-related proteins such as microtubule-associated protein light chain 3 I and II (LC3I/II).…”

Section: Roles Of Pcbps In Hematological Malignanciesmentioning

confidence: 99%

Poly(rC)-binding proteins as pleiotropic regulators in hematopoiesis and hematological malignancy

et al. 2022

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Poly(rC)-binding proteins (PCBPs), a defined subfamily of RNA binding proteins, are characterized by their high affinity and sequence-specific interaction with poly-cytosine (poly-C). The PCBP family comprises five members, including hnRNP K and PCBP1-4. These proteins share a relatively similar structure motif, with triple hnRNP K homology (KH) domains responsible for recognizing and combining C-rich regions of mRNA and single- and double-stranded DNA. Numerous studies have indicated that PCBPs play a prominent role in hematopoietic cell growth, differentiation, and tumorigenesis at multiple levels of regulation. Herein, we summarized the currently available literature regarding the structural and functional divergence of various PCBP family members. Furthermore, we focused on their roles in normal hematopoiesis, particularly in erythropoiesis. More importantly, we also discussed and highlighted their involvement in carcinogenesis, including leukemia and lymphoma, aiming to clarify the pleiotropic roles and molecular mechanisms in the hematopoietic compartment.

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Section: Roles Of Pcbps In Hematological Malignanciesmentioning

confidence: 99%

Poly(rC)-binding proteins as pleiotropic regulators in hematopoiesis and hematological malignancy

et al. 2022

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“…Acute promyelocyte leukaemia ranks first among malignant diseases occurring in young people [3]. During the pathological process of APL, leukaemia cells uncontrollably proliferate in the bone marrow and other haematopoietic tis-sues and then enter the peripheral blood to inhibit the proliferation of normal cells [4,5]. Multiple risk factors, such as viruses, genetic predisposition, chemical poisons, radiation, and drugs, can lead to APL [6].…”

Section: Introductionmentioning

confidence: 99%

MIR-320a/b inhibits cell viability and cell cycle progression by targeting aryl hydrocarbon receptor nuclear translocator-like in acute promyelocyte leukaemia

Hu¹,

Shen²,

Ye³

2022

pjp

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Acute promyelocyte leukaemia (APL) is a subgroup of acute myeloid leukaemia. Dysregulation of clock genes has been revealed to be involved in APL progression. Herein, the mechanism of clock gene aryl hydrocarbon receptor nuclear translocatorlike (ARNTL) in APL was explored. The expression of ARNTL, period circadian regulator 1 and 2 (PER1 and PER2) in APL tissue samples and normal samples was analysed by bioinformatic analysis. Gene expression in APL cells was detected by reverse transcription quantitative polymerase chain reaction. Acute promyelocyte leukaemia cell viability and cell cycle progression were assessed by cell counting kit 8 (CCK-8) assays and flow cytometry analyses, respectively. The protein levels of ARNTL and cell cycle markers were examined by western blotting. Interaction between ARNTL and miR-320a/b was confirmed by luciferase reporter assays. Aryl hydrocarbon receptor nuclear translocator-like was overexpressed in marrow tissues of patients with acute myeloid leukaemia and predicted poor outcome. Aryl hydrocarbon receptor nuclear translocator-like knockdown inhibited APL cell viability and arrested APL cells in the G1 phase. Mechanically, ARNTL was targeted by miR-320a/b. Moreover, miR-320a/b upregulation promoted cell cycle arrest in the G1 phase and suppressed the viability of APL cells, and the impacts were reversed by ARNTL overexpression. In conclusion, miR-320a/b suppresses cell viability and leads to cell cycle arrest by suppressing ARNTL in APL.

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Heterogeneous nuclear ribonucleoprotein K is overexpressed in acute myeloid leukemia and causes myeloproliferation in mice via altered Runx1 splicing

et al. 2022

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Acute myeloid leukemia (AML) is driven by numerous molecular events that contribute to disease progression. Herein, we identify hnRNP K overexpression as a recurrent abnormality in AML that negatively correlates with patient survival. Overexpression of hnRNP K in murine fetal liver cells results in altered self-renewal and differentiation potential. Further, murine transplantation models reveal that hnRNP K overexpression results in myeloproliferation in vivo. Mechanistic studies expose a direct functional relationship between hnRNP K and RUNX1—a master transcriptional regulator of hematopoiesis often dysregulated in leukemia. Molecular analyses show that overexpression of hnRNP K results in an enrichment of an alternatively spliced isoform of RUNX1 lacking exon 4. Our work establishes hnRNP K’s oncogenic potential in influencing myelogenesis through its regulation of RUNX1 splicing and subsequent transcriptional activity.

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Crosstalk between hnRNP K and SET in ATRA‐induced differentiation in acute promyelocytic leukemia

Cited by 4 publications

References 49 publications

Poly(rC)-binding proteins as pleiotropic regulators in hematopoiesis and hematological malignancy

Poly(rC)-binding proteins as pleiotropic regulators in hematopoiesis and hematological malignancy

MIR-320a/b inhibits cell viability and cell cycle progression by targeting aryl hydrocarbon receptor nuclear translocator-like in acute promyelocyte leukaemia

Heterogeneous nuclear ribonucleoprotein K is overexpressed in acute myeloid leukemia and causes myeloproliferation in mice via altered Runx1 splicing

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