Similar Datasets
Project description:To investigate the changes in gene expression during the process of differentiation into neutrophils, microarray analysis was performed. HL-60 cells were cultured with all-trans retinoic acid (ATRA) for 4 days. The cells were collected at four different time points and total RNA was prepared for use as a sample for microarray analysis.
2022-12-28 | GSE200823 | GEO
Project description:To investigate the changes in gene expression during the process of differentiation into eosinophils, microarray analysis was performed. HL-60 clone 15 cells were cultured with apicidin for 6 days. The cells were collected at four different time points and total RNA was prepared for use as a sample for microarray analysis.
2022-12-28 | GSE200826 | GEO
Project description:To investigate the changes in gene expression during the process of differentiation into neutrophils and to evaluate the effect of Ak2 hetero-knockout in the process, microarray analysis was performed. HL-60 Ak2 hetero-knockout clone #47 cells were cultured with all-trans retinoic acid (ATRA) for 4 days. The cells were collected at four different time points and total RNA was prepared for use as a sample for microarray analysis.
2022-12-28 | GSE200825 | GEO
Project description:To investigate the changes in gene expression during the process of differentiation into neutrophils and to evaluate the effect of Ak2 hetero-knockout in the process, microarray analysis was performed. HL-60 Ak2 hetero-knockout clone #5 cells were cultured with all-trans retinoic acid (ATRA) for 4 days. The cells were collected at four different time points and total RNA was prepared for use as a sample for microarray analysis.
2022-12-28 | GSE200824 | GEO
Project description:The human myeloid leukemia cell line HL-60 differentiate into monocytes following treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the mechanism underlying the differentiation of these cells in response to TPA has not been fully elucidated. In this study, we performed ChIP-seq profiling of RNA Pol II, HDAC2, Acetyl H3 (AcH3), and H3K27me3 and analyzed differential chromatin state changes during TPA-induced differentiation of HL-60 cells. We focused on atypically active genes, which showed enhanced H3 acetylation despite increased HDAC2 recruitment. We found that HDAC2 positively regulates the expression of these genes in a histone deacetylase activity-independent manner. HDAC2 interacted with and recruited paired box 5 (PAX5) to the promoters of the target genes and regulated HL-60 cell differentiation by PAX5-mediated gene activation. Taken together, these data elucidated the specific-chromatin status during HL-60 cell differentiation following TPA exposure and suggested that HDAC2 can activate transcription of certain genes through interactions with PAX5 in a deacetylase activity-independent pathway.
| S-EPMC6108480 | biostudies-literature
Project description:We have adopted a special experimental strategy to identify early responsive genes during 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced macrophage-like differentiation of human myeloid leukemia cells (HL-60). This was performed in cells that were synchronized by nocodazole and treated with TPA in the presence of a protein synthesis inhibitor, cycloheximide, to prevent activation of secondary targets and therefore increase the probability of early transcripts in total RNA pool. The expression alteration was analyzed by microarray and the selection criteria of candidate genes were adjusted by real-time PCR validation to increase its reliability. Finally, 56 genes were identified as early TPA-responsive genes in this multiscreening step approach. Furthermore, upregulation of three candidate genes (NFIL3, SKIL, and JMJD3) was shown to be dosage and time dependent with TPA treatment and was found to be directly regulated by TPA through PKC-dependent signaling. These results revealed that our screenings provide a useful and efficient approach to identify early TPA-responsive genes and these genes might involve the regulation of TPA-induced differentiation program of HL-60 cells as primary
| S-EPMC6032445 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-11-26 | GSE124423 | GEO
Project description:Studies have shown that nuclear translocation of actin occurs under certain conditions of cellular stress; however, the functional significance of actin import remains unclear. Here, we demonstrate that during the phorbol 12-myristate 13-acetate (PMA)-induced differentiation of HL-60 cells toward macrophages, beta-actin translocates from the cytoplasm to the nucleus and that this process is dramatically inhibited by pretreatment with p38 mitogen-activated protein kinase inhibitors. Using chromatin immunoprecipitation-on-chip assays, the genome-wide maps of beta-actin binding to gene promoters in response to PMA treatment is analyzed in HL-60 cells. A gene ontology-based analysis shows that the identified genes belong to a broad spectrum of functional categories such as cell growth and differentiation, signal transduction, response to external stimulus, ion channel activity, and immune response. We also demonstrate a correlation between beta-actin occupancy and the recruitment of RNA polymerase II at six selected target genes, and beta-actin knockdown decreases the mRNA expression levels of these target genes induced by PMA. We further show that nuclear beta-actin is required for PMA-induced transactivation of one target gene, solute carrier family 11 member 1, which is important for macrophage activation. Our data provide novel evidence that nuclear accumulation of beta-actin is involved in transcriptional regulation during macrophage-like differentiation of HL-60 cells.
| S-EPMC2828967 | biostudies-literature
Project description:In this study, we present an effective model All-Trans Retinoic Acid (ATRA)-induced differentiation of HL-60 cells. The model describes reinforcing feedback between an ATRA-inducible signalsome complex involving many proteins including Vav1, a guanine nucleotide exchange factor, and the activation of the mitogen activated protein kinase (MAPK) cascade. We decomposed the effective model into three modules; a signal initiation module that sensed and transformed an ATRA signal into program activation signals; a signal integration module that controlled the expression of upstream transcription factors; and a phenotype module which encoded the expression of functional differentiation markers from the ATRA-inducible transcription factors. We identified an ensemble of effective model parameters using measurements taken from ATRA-induced HL-60 cells. Using these parameters, model analysis predicted that MAPK activation was bistable as a function of ATRA exposure. Conformational experiments supported ATRA-induced bistability. Additionally, the model captured intermediate and phenotypic gene expression data. Knockout analysis suggested Gfi-1 and PPARg were critical to the ATRAinduced differentiation program. These findings, combined with other literature evidence, suggested that reinforcing feedback is central to hyperactive signaling in a diversity of cell fate programs.
| S-EPMC5662654 | biostudies-literature
Project description:The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is a potent inducer of differentiation in human promyelocytic leukemia cells. Recently, TPA has been successfully administered to patients with myelocytic leukemia and has produced therapeutic effects that led to temporary remission. These studies demonstrated the potential efficacy of TPA in cancer chemotherapy. We now seek to understand the biological effects and molecular mechanisms of differentiation in response to TPA treatment in leukemia cells by expression profiling using DNA microarray. Our results show distinct temporal and coordinated gene changes that are consistent with differentiation and activation of multiple biochemical pathways in HL-60 cells exposed to TPA. Alterations of gene expression in HL-60 cells include various transcription factors, cytokines and protein markers that are consistent with the induction of differentiation elicited by TPA. These temporal patterns of gene expression were abolished or greatly diminished in an HL-60 derived TPA- resistant variant cell line (HL-525), thus revealing transcriptional and consequential biochemical changes that may be required for TPA-induced differentiation. In addition, certain genes were upregulated by TPA in TPA-resistant HL-525 cells but not in TPA-sensitive HL-60 cells suggesting that these genes may play a role in the resistant phenotype. These patterns of gene expression may be important for predicting response to TPA.
| S-EPMC137144 | biostudies-literature