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Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [array]

ABSTRACT: Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [array]

PROVIDER: PRJNA915607 | ENA |

REPOSITORIES: ENA

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Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [array]

Project description:Cytarabine is the main drug for acute myeloid leukemia (AML) treatment; however, drug resistance hinders the treatment of AML. Although microRNA (miRNA) alteration is one of the well-recognized mechanisms underlying drug resistance in AML, few studies have investigated the role and function of miRNAs in the development of cytarabine resistance. In this study, total RNA was isolated from parental HL60 and cytarabine resistant HL60 (R-HL60) cells. Subsequently, miRNAs and mRNAs were detected using small RNA sequencing and gene expression array, respectively. The miRNAs and genes with ≥ 2-fold difference in expression between HL60 and R-HL60 cells were screened out. Negatively correlated miRNA–mRNA pairs were selected as candidate miRNA–mRNA target pairs by using the miRDB, Targetscan or miRTar databases. Functional enrichment analysis of differentially expressed genes (DEGs) included in the candidate miRNA–mRNA network was performed. The results revealed that CCL2, SOX9, SLC8A1, ICAM1, CXCL10, SIPR2, FGFR1, OVOL2, MITF, and CARD10 were simultaneously involved in seven GO pathways, namely the regulation of cell migration, regulation of locomotion, regulation of cellular component movement, cell migration, locomotion, cell motility, localization of cell. These genes were negatively correlated with the altered miRNAs (miR-1-3p, miR-155-5p, miR-1255b-5p, miR-200c-5p, miR-3609, miR-1285-3p, miR-124-3p, miR-146a-5p, miR-497a-5p, and miR-3150a-5p), suggesting that they are the potential targets of the miRNAs to regulate cell migration behavior or ability. Therefore, our results advance our understanding of the regulatory mechanism underlying cytarabine resistance development, specifically related to miRNAs.

2023-12-03 | GSE221718 | GEO

Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [miRNA-seq]

2023-12-03 | GSE221717 | GEO

Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells

Project description:Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells

| PRJNA915605 | ENA

Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [miRNA-seq]

Project description:Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells [miRNA-seq]

| PRJNA915606 | ENA

Identification of potential miRNA–mRNA regulatory network contributing to cytarabine resistance HL60 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-03 | GSE221719 | GEO

microRNA array analysis of differentiated HL60 cells with PfbA

Project description:microRNA array analysis of differentiated HL60 cells with PfbA

| PRJNA527201 | ENA

comparison of HL60-NG cell and HL60-RG cell

Project description:Human Promyelocytic Leukemia Cell Line HL60 has been used extensively as a model for myeloid differentiation and leukemia. HL60-RG cell is its sub-line and shows a higher growth rate. In this study, we carried out a genome scan using SNP 10k mapping array on both cells. Comparative study on chromosomal changes of these cells will give us information on mechanism of tumor progression. Keywords: cell type comparison

2008-01-04 | GSE10060 | GEO

Transcription profiling of human leukemia HL60-NG cell and HL60-RG cell

2008-06-17 | E-GEOD-10060 | biostudies-arrayexpress

Hi-C detects novel rearrangements in HL60 and HL60/S4 cell lines

Project description:Hi-C detects novel rearrangements in HL60 and HL60/S4 cell lines

2018-12-02 | GSE120815 | GEO

Prediction of miRNA‑mRNA network regulating the migration ability of cytarabine‑resistant HL60 cells.

Project description:Cytarabine is an important medicine for acute myeloid leukemia (AML) treatment, however, drug resistance hinders the treatment of AML. Although microRNA (miRNA or miR) alteration is one of the well-recognized mechanisms underlying drug resistance in AML, few studies have investigated the role and function of miRNAs in the development of cytarabine resistance. In the present study, total RNA was isolated from parental HL60 and cytarabine-resistant HL60 (R-HL60) cells. Subsequently, miRNAs and mRNAs were detected using small RNA sequencing and gene expression array, respectively. Differentially expressed mRNAs (DEMs) and differentially expressed genes (DEGs) with more than two-fold changes between HL60 and R-HL60 cells were screened out. Negatively associated miRNA-mRNA pairs were selected as candidate miRNA-mRNA target pairs according to the miRDB, Targetscan or miRTar databases. Functional enrichment analysis of DEGs included in the candidate miRNA-mRNA pairs was performed. The results indicated that 10 DEGs (CCL2, SOX9, SLC8A1, ICAM1, CXCL10, SIPR2, FGFR1, OVOL2, MITF and CARD10) were simultaneously involved in seven Gene Ontology pathways related to the regulation of migration ability, namely the 'regulation of cell migration', 'regulation of locomotion', 'regulation of cellular component movement', 'cell migration', 'locomotion', 'cell motility', and 'localization of cell'. DEMs predicted to negatively regulate the aforementioned 10 DEGs were paired with DEGs into 16 candidate miRNA-mRNA pairs related to the regulation of migration ability. In addition, migration assays revealed that the migration ability of R-HL60 cells was greater than that of HL60 cells. These findings provide a new perspective for the treatment of cytarabine-resistant AML and advance our understanding of altered migration ability underlying cytarabine resistance development, specifically related to miRNAs.

| S-EPMC10758919 | biostudies-literature

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