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Shotgun mass-spectrometry of HL-60 cell proteins for spectrum library development

ABSTRACT: ATRA-induced differentiation of HL-60 cells was studied using targeted mass-spectrometry including selected reaction monitoring (SRM) and parallel reaction monitoring (PRM) approach. PRM experiment was performed in time-course manner, without peptide standards usage. PRM data was inspected in Skyline 3.1 software. In order to check peptide identity we developed spectrum library based on shotgun mass-spectrometry data, which has been obtained for HL-60 cells protein samples at 0, 3, 24, 48 and 96h after ATRA treatment.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Acute Leukemia

SUBMITTER: Svetlana Novikova

LAB HEAD: Victor Zgoda

PROVIDER: PXD006421 | Pride | 2017-11-09

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	FASP_HL60_0h1.mgf	Mgf
	FASP_HL60_0h1.mzid.gz	Mzid
	FASP_HL60_0h1.pride.mgf.gz	Mgf
	FASP_HL60_0h1.pride.mztab.gz	Mztab
	FASP_HL60_0h1.raw	Raw

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Publications

Application of selected reaction monitoring and parallel reaction monitoring for investigation of HL-60 cell line differentiation.

Novikova Svetlana E SE Tikhonova Olga V OV Kurbatov Leonid K LK Farafonova Tatiana E TE Vakhrushev Igor V IV Zgoda Victor G VG

European journal of mass spectrometry (Chichester, England) 20170801 4

Targeted mass spectrometry represents a powerful tool for investigation of biological processes. The convenient approach of selected reaction monitoring using stable isotope-labeled peptide standard (SIS) is widely applied for protein quantification. Along with this method, high-resolution parallel reaction monitoring has been increasingly used for protein targeted analysis. Here we applied two targeted approaches (selected reaction monitoring with SIS and label-free parallel reaction monitoring ...[more]

PMID: 29028392

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Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

Project description:Transcriptional profiling of human leukemia?HL-60 cells comparing ATRA treated HL-60 cells with ATRA plus ATO. Goal was to determine the effects of ATO on ATRA induced differentiation of HL-60 cells. Two-condition experiment, ATRA vs. ATRA plus ATO treated HL-60 cells.

2015-03-31 | E-GEOD-67420 | biostudies-arrayexpress

Time-coursed transcriptomics of ATRA-induced granulocytic differentiation

Project description:Transcriptional profiling of HL-60 cells at 0, 3, 24, and 96 h after ATRA treatment. The differentially expressed genes was meant to be the input data for bioinformatic upstream regulator search

2021-09-01 | E-MTAB-10606 | biostudies-arrayexpress

Proteome dynamics of HL-60, NB4, and K562 cells under the ATRA treatment

Project description:Searching for new strategies of acute myeloid leukemia (AML) treatment is of particular interest. Cell lines, e. g. HL-60 and NB4, represent model systems to study molecular features of leukemic cells. The all-trans-retinoic acid (ATRA) has proven itself to be an effective treatment for one of AML subtypes, i.e., acute promyelocytic leukemia (APL). At the same time, ATRA causes granulocytic differentiation of non-APL leukemic cells in vitro. Combination of new therapeutics with ATRA could improve efficiency of treatment. Studying the proteome perturbation in leukemic cells under the ATRA treatment allows to determine potential regulatory molecules that could be affected pharmacologically. Thus, the TMT-based proteomic profiles of HL-60, NB4, and K562 cell lines under the ATRA treatment were obtained at 0, 3, 12, 24, and 72 h after the ATRA treatment.

2024-06-23 | PXD050317 | Pride

The Study of ATRA-Induced Differentiation of the HL-60 Cell Line

Project description:Shotgun mass-spectrometric experiment was performed with HL-60 cells induced to differentiation at 0, 3, 24, 48 and 96h after ATRA treatment. Obtained data has been used for label-free quantification by SPIRE platform based on spectral count. Results on proteome profiling were used for up-stream regulator search in geneXplain platform (http://genexplain.com/).

2021-09-07 | PXD006768 | Pride

Expression profiling of myeloid leukemia cell treated with vibsanine A, PMA and ATRA

Project description:All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanine A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanine A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanine A, PMA, and ATRA. HL-60 cells were treated with vibsanine A, PMA and ATRA for 6 hours or longer up to 24 hours. Gene expression profiling was conducted

2016-02-28 | E-GEOD-78734 | biostudies-arrayexpress

Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

Project description:Transcriptional profiling of human leukemia　HL-60 cells comparing ATRA treated HL-60 cells with ATRA plus ATO. Goal was to determine the effects of ATO on ATRA induced differentiation of HL-60 cells.

2015-03-31 | GSE67420 | GEO

RNA seq of HL-60 cells in untreated, ATRA (All- trans retinoic acid) and Vitamin D3 treated conditions

Project description:The leukemic cell line HL-60 is widely used to study normal and aberrant myelopoiesis. HL-60 cells can be treated with ATRA (all-trans retinoic acid) and Vit-D3 (1,25-Dihydroxyvitamin D3, calcitriol) to differentiate into granulocytes and monocytes respectively. Induced myeloid differentiation helps us to understand the molecular basis of myeloid differentiation. To understand the genome-wide gene expression changes associated with HL-60 cells upon myeloid differentiation, RNA-sequencing was carried out. We subjected the HL-60 cells with 10 µM ATRA and 50 nM Vit-D3 for 72 hours. Post induction, the uninduced and induced cells were sorted based on CD11b and CD14 markers. The uninduced cells were negative for both the markers while ATRA and Vit D3 inductions were highly positive for CD11b-FITC and CD14-APC-H7 markers respectively. Two biological replicates were used for this experiment. Sorted cells were collected for RNA extraction using RNAeasy Kit from Qiagen and RNA quality was assessed using Bioanalyzer. High quality RNA with RIN values greater than 8, were used to generate library using TrueSeq stranded library preparation kit from Illumina following manufacturer’s instructions. Finally, barcoded libraries were pooled, and a final concentration of 10 nM was loaded in HiSeq 2500 Illumina platform and paired-end sequencing for 2*126 cycles were carried out.

2023-01-25 | E-MTAB-12267 | biostudies-arrayexpress

Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [Illumina HumanHT-12 gene expression array]

Project description:All-trans-retinoic acid (ATRA) has been successfully used in therapy of acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML) but the response of non-APL AML cases to ATRA-based treatment has been poor. Here we show that, via epigenetic reprogramming, inhibitors of LSD1/KDM1 demethylase including tranylcypromine (TCP) unlocked the ATRA-driven therapeutic response in non-APL AML. LSD1 inhibition did not lead to an increase in genome-wide H3 lysine4 dimethylation (H3K4me2) but did increase H3K4me2 and expression of myeloid differentiation-associated genes. Importantly, treatment with ATRA plus TCP dramatically diminished engraftment of primary human AML cells in vivo in NOD.SCID mice, suggesting that ATRA in combination with TCP may target leukemia-initiating cells. Furthermore, initiation of ATRA plus TCP co-treatment 15 days post-engraftment of human AML cells in NOD.SCID gamma mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect, which was superior to treatment with either drug alone. These data identify LSD1 as a therapeutic target and strongly suggest that it may contribute to AML pathogenesis by inhibiting the normal pro-differentiative function of ATRA, paving the way for novel combinatorial therapies of AML. Overall, 30 specimens derived from HL-60 or TEX cell line were treated with drugs and hybridized to Illumina HumanHT-12 gene expression arrays.

2012-03-14 | E-GEOD-34672 | biostudies-arrayexpress

Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [ChIP-Seq]

Project description:All-trans-retinoic acid (ATRA) has been successfully used in therapy of acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML) but the response of non-APL AML cases to ATRA-based treatment has been poor. Here we show that, via epigenetic reprogramming, inhibitors of LSD1/KDM1 demethylase including tranylcypromine (TCP) unlocked the ATRA-driven therapeutic response in non-APL AML. LSD1 inhibition did not lead to an increase in genome-wide H3 lysine4 dimethylation (H3K4me2) but did increase H3K4me2 and expression of myeloid differentiation-associated genes. Importantly, treatment with ATRA plus TCP dramatically diminished engraftment of primary human AML cells in vivo in NOD.SCID mice, suggesting that ATRA in combination with TCP may target leukemia-initiating cells. Furthermore, initiation of ATRA plus TCP co-treatment 15 days post-engraftment of human AML cells in NOD.SCID gamma mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect, which was superior to treatment with either drug alone. These data identify LSD1 as a therapeutic target and strongly suggest that it may contribute to AML pathogenesis by inhibiting the normal pro-differentiative function of ATRA, paving the way for novel combinatorial therapies of AML. ChIP-seq was used to study the effects of ATRA, TCP and ATRA/TCP treatment on H3K4 dimethylation. In addition to the three treatment samples, two reference samples were processed: (i) An untreated sample using the same anti-H3K4me2 antibody and an untreated sample using IgG. These five sequencing experiments were conducted using HL-60 cells and TEX cells, leading to 10 ChIP-seq samples in total.

2012-03-14 | E-GEOD-34725 | biostudies-arrayexpress

RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion and the inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance

Project description:GTF2I-RARA is a newly identified RARA fusion gene in variant acute promyelocytic leukemia (APL) with t(7;17)(q11;q21). Clinical manifestation in the patient showed that it is a sort of ATRA-insensitive oncogene and is different from the classic PML-RARA in terms of therapeutic reaction. To reveal the functional characteristics and regulating mechanism of the GTF2I-RARA fusion gene, we established a GTF2I-RARA-transfected HL-60 cell model and confirmed its resistance to ATRA. Compared with PML-RARA, GTF2I-RARA has a higher affinity to HDAC3 under the treatment of ATRA. Using the ChIP-sequencing approach, we identified 221 GTF2I-RARA binding sites in model cells, and found that the RING finger protein 8(RNF8) is a target gene of GTF2I-RARA, which participated in the disease progression and therapy resistance in APL with GTF2I-RARA transcript. The elevated RNF8 expression promotes the interaction between RARA and RNF8 and induced RARA ubiquitylation and degradation, resulting in attenuated transcriptional activation of RARA. Our results suggested that RNF8 is a key GTF2I-RARA downstream event. Using the combination of MG132 and ATRA to treat the GTF2I-RARA-HL-60 cells, a synergistic effect leading to GTF2I-RARA-HL-60 cell differentiation was confirmed. Taken together, the targeting of RNF8 may be an alternative choice for treatment in variant APL with GTF2I-RARA fusion.

2018-11-10 | GSE122354 | GEO

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