Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Baxter, Shaneen S.; Carlson, Leonard A.; Mayer, Alejandro M. S.; Hall, Melanie; Fay, Mike

doi:10.1007/s11626-008-9163-4

Cited by 17 publications

(13 citation statements)

References 63 publications

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“…At 24 and 72 h after stimulation with ADM , Cul5 mRNA increased 1.35-and 4.18-fold, respectively, in primed cells vs. resting cultures. Our data were in agreement with the increase of Cul5 mRNA and protein detected by Baxter et al (19) during ATRA-mediated differentiation of HL60 cells.…”

Section: Resultssupporting

confidence: 93%

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Adrenomedullin in the growth modulation and differentiation of acute myeloid leukemia cells

Liddo

Bridi

Gottardi

et al. 2016

International Journal of Oncology

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Abstract. Adrenomedullin (ADM) is a regulatory peptide endowed with multiple biological effects, including the regulation of blood pressure, cell growth and innate host defence. In the present study, we demonstrated that ADM signaling could be involved in the impaired cellular differentiation of myeloid leukemia cells to mature granulocytes or monocytes by modulating RAMPs/CRLR expression, PI3K/Akt cascade and the ERK/MAPK signaling pathway. When exogenously administered to in vitro cultures of HL60 promyelocytic leukemia cells, ADM was shown to exert a strong proliferative effect with minimal upregulation in the expression level of monocyte antigen CD14. Notably, the experimental inhibition of ADM signaling with inhibitor ADM 22-52 promoted a differentiative stimulation towards monocytic and granulocytic lineages. Moreover, based on the expression of CD31 relative to CD38, we hypothesized that an excess of ADM in bone marrow (BM) niche could increase the transendothelial migration of leukemia cells while any inhibitory event of ADM activity could raise cell retention in hyaluronate matrix by upregulating CD38. Taken into consideration the above evidence, we concluded that ADM and ADM 22-52 could differently affect the growth of leukemia cells by autocrine/paracrine mechanisms and may have clinical relevance as biological targets for the intervention of tumor progression.

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Section: Resultssupporting

confidence: 93%

“…Thus, the proliferative and differentiative effects induced by ADM and its inhibitor, ADM , were evaluated in vitro at different time-points in HL60 cells, a human promyelocytic leukaemia cell line widely used to study granulocyte differentiation (19).…”

Section: Introductionmentioning

confidence: 99%

Adrenomedullin in the growth modulation and differentiation of acute myeloid leukemia cells

Liddo

Bridi

Gottardi

et al. 2016

International Journal of Oncology

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“…As an additional validation of the µParaflo™ microRNA microarray assay, the expression of miR-423-5p (rno481159_mir) was examined by real-time PCR since the expression of this miRNA was not significantly altered with Cd treatment. The fold change in miRNA expression between saline control and Cd-treated samples was determined using the comparative CT method as previously described using QuantStudio™ Design Analysis Software (Version 1.4, Applied Biosystems by Thermo Fisher Scientific, Carlsbad, CA, USA, 2016) [ 29 , 30 ]. Statistical analysis was performed on the 2 −ΔCT values using an unpaired t -test ( N = 6 per group, p ≤ 0.05) with GraphPad Prism software (Version 7.00, GraphPad Software Inc., La Jolla, CA, USA, 2016).…”

Section: Methodsmentioning

confidence: 99%

Cadmium Nephrotoxicity Is Associated with Altered MicroRNA Expression in the Rat Renal Cortex

Fay

Alt

Ryba

et al. 2018

Toxics

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Cadmium (Cd) is a nephrotoxic environmental pollutant that causes a generalized dysfunction of the proximal tubule characterized by polyuria and proteinuria. Even though the effects of Cd on the kidney have been well-characterized, the molecular mechanisms underlying these effects have not been fully elucidated. MicroRNAs (miRNAs) are small non-coding RNAs that regulate cellular and physiologic function by modulating gene expression at the post-transcriptional level. The goal of the present study was to determine if Cd affects renal cortex miRNA expression in a well-established animal model of Cd-induced kidney injury. Male Sprague-Dawley rats were treated with subcutaneous injections of either isotonic saline or CdCl2 (0.6 mg/kg) 5 days a week for 12 weeks. The 12-week Cd-treatment protocol resulted in kidney injury as determined by the development of polyuria and proteinuria, and a significant increase in the urinary biomarkers Kim-1, β2 microglobulin and cystatin C. Total RNA was isolated from the renal cortex of the saline control and Cd treated animals, and differentially expressed miRNAs were identified using µParafloTM microRNA microarray analysis. The microarray results demonstrated that the expression of 44 miRNAs were significantly increased and 54 miRNAs were significantly decreased in the Cd treatment group versus the saline control (t-test, p ≤ 0.05, N = 6 per group). miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p demonstrated more abundant expression and a significant two-fold or greater increased expression in the Cd-treatment group versus the saline control group. miR-193b-3p, miR-455-3p, and miR-342-3p demonstrated more abundant expression and a significant two-fold or greater decreased expression in the Cd-treatment group versus the saline control group. Real-time PCR validation demonstrated (1) a significant (t-test, p ≤ 0.05, N = 6 per group) increase in expression in the Cd-treated group for miR-21-5p (2.7-fold), miR-34a-5p (10.8-fold), miR-146b-5p (2-fold), miR-224-5p (10.2-fold), miR-3084a-3p (2.4-fold), and miR-3084c-3p (3.3-fold) and (2) a significant (t-test, p ≤ 0.05, N = 6 per group) 52% decrease in miR-455-3p expression in the Cd-treatment group. These findings demonstrate that Cd significantly alters the miRNA expression profile in the renal cortex and raises the possibility that dysregulated miRNA expression may play a role in the pathophysiology of Cd-induced kidney injury. In addition, these findings raise the possibility that Cd-dysregulated miRNAs might be used as urinary biomarkers of Cd exposure or Cd-induced kidney injury.

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“…Cul5 mRNA and protein levels are decreased in the rat cerebral cortex and hippocampus in response to traumatic brain injury (TBI) [ 44 ]. Another report showed a 6.5-fold upregulation of Cul5 associated with granulocytic differentiation of HL-60 cells [ 45 ].…”

Section: Identification and Regulation Of Cullinmentioning

confidence: 99%

The role of cullin 5-containing ubiquitin ligases

et al. 2016

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The suppressor of cytokine signaling (SOCS) box consists of the BC box and the cullin 5 (Cul5) box, which interact with Elongin BC and Cul5, respectively. SOCS box-containing proteins have ubiquitin ligase activity mediated by the formation of a complex with the scaffold protein Cul5 and the RING domain protein Rbx2, and are thereby members of the cullin RING ligase superfamily. Cul5-type ubiquitin ligases have a variety of substrates that are targeted for polyubiquitination and proteasomal degradation. Here, we review the current knowledge on the identification of Cul5 and the regulation of its expression, as well as the signaling pathways regulated by Cul5 and how viruses highjack the Cul5 system to overcome antiviral responses. Identification and regulation of cullin 5Cullin 5 (Cul5) was originally identified as a vasopressin-activated calcium-mobilizing (VACM-1) protein, an arginine vasopressin (AVP) receptor [1]. AVP is a nonapeptide that regulates body fluid and blood pressure homeostasis. VACM-1 is recognized as Cul5 because of its homology to the Caenorhabditis elegans gene Cul5 [2,3]. Cul5 is expressed in many cells and organs, including endothelial cells, brain, kidney collecting tubule cells, and vascular endothelial cells [2,[4][5][6]7]. Cul5 inhibits cyclic AMP production, and this effect is reversed by staurosporin, a protein kinase A (PKA) inhibitor, or by mutating S730A, the PKA-dependent phosphorylation site in the Cul5 sequence in COS-1 cells [8]. The inhibitory effect of Cul5 on AVP-stimulated cAMP production is enhanced by a protein kinase C inhibitor [8]. CUL-5 expression is downregulated in 82 % (41/50) of breast tumors compared with matched normal tissues [9]. Overexpression of Cul5 in T47D breast cancer cells decreases cell growth and mitogen activated protein kinase (MAPK) phosphorylation [10], and Cul5 overexpression downregulates early growth response 1 (EGR-1) protein expression and upregulates Fas-L mRNA expression [10]. The regulation of both MAPK and EGR-1 pathways by 17β-estradiol led to the examination of estrogen-dependent T47D cell growth, which showed that Cul5 inhibits basal and 17β-estradiol-dependent cell growth and MAPK phosphorylation [11].Resveratrol (trans-3,5,4′-trihydroxystilbene), which inhibits tumor initiation and promotion, is a natural component of the human diet, and its wide range of biological activities has been demonstrated in vivo and in vitro [12][13][14][15]. The antiproliferative effect of resveratrol is significantly enhanced by Cul5 overexpression in T47D cells [16].The expression of Cul5 is regulated by several stimuli and pathways (Fig. 1). Resveratrol upregulates Cul5 expression and decreases T47D cell growth, suggesting that the antiproliferative effect of resveratrol is mediated by Cul5 [16]. Cul5 is a flexible scaffold protein with a preferred distribution of conformational states [17], and NEDD8 modification (neddylation) alters the conformation of Cul5 and activates it [18]. Cul5(S730A) accelerates cellular proliferation and induces an...

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Granulocytic differentiation of HL-60 promyelocytic leukemia cells is associated with increased expression of Cul5

Cited by 17 publications

References 63 publications

Adrenomedullin in the growth modulation and differentiation of acute myeloid leukemia cells

Adrenomedullin in the growth modulation and differentiation of acute myeloid leukemia cells

Cadmium Nephrotoxicity Is Associated with Altered MicroRNA Expression in the Rat Renal Cortex

The role of cullin 5-containing ubiquitin ligases

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