RNAseq of control and GFI1-expressing A549
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ABSTRACT:
PROVIDER: PRJNA694048 | ENA |
REPOSITORIES: ENA
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Project description:To study the effect of transcription factor GFI1 on lung cancer cells, we overexpressed GFI1 in A549 cells and performed RNA-seq. Moreover, control and GFI1-expressing A549 cells that were forced into suspension for 48hrs were used performed RNA-seq.
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Project description:To investigate the genes regulated by the transcription factor GFI1 in lung cancer cells, we overexpressed GFI1-Flag in A549 cells and performed ChIP-Seq with anti-Flag affinity gel.
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Project description:GFI1 is a transcriptional repressor that plays an essential role in HSCs development, lymphoid and myeloid differentiation and Acute Myeloid Leukemia (AML) pathogenesis. Low expression of Gfi1 leads to poor prognosis in AML patients and is associated with less overall survival in murine AML models. In the current study, we show that mice with a low level or loss of GFI1 expression resulted in significantly fewer HSCs compared to normal GFI1 expression. We also show that, in a competitive transplantation setup involving cells expressing low and normal GFI1 levels, HSCs with a low level of GFI1 expression reconstituted the bone marrow (BM) including the HSCs, progenitors and differentiated cells. In contrast, HSCs with the complete loss of GFI1 failed to regenerate BM in competition with cells expressing normal GFI1 levels. To further investigate the molecular changes, we performed RNAseq analysis in HSCs derived from wildtype (GFI1-KI), low-level (GFI1-KD), loss (Gfi1-KO) and Gfi1 mutant (GFI1-36N) mice. In the pathway analysis, we observed a significant upregulation of cell-cycle-related pathways in HSCs derived from mice expressing low-level and mutant variant (36N) of GFI1., Strikingly, these pathways are significantly downregulated in the HSCs of GFI1-KO mice.
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Project description:RNAseq of wildtype and GFI1-KO H1155
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Project description:GFI1 is a transcriptional repressor protein that plays an essential role in HSCs development, lymphoid and myeloid differentiation and Acute Myeloid Leukaemic (AML) pathogenesis. Low expression levels of GFI1 is associated with a poor prognosis in AML development. In addition, a single nucleotide polymorphism (SNP) variant of GFI1 results in the generation of GFI1 protein with asparagine (N) instead of serine (S) at the 36th amino acid position, known as GFI136N. Expression of the GFI1-36N allele leads as well to poor prognosis and promotes AML development. In this study, we demonstrated with the help of RNAseq transcriptomic analysis that the presence of GFI1-36N is associated with increased frequency of chromosomal aberrations and mutational burden in murine and human AML cells. In particular, GFI1-36N modulates DNA repair pathways, O6-methylguanine-DNA-methyltransferase (MGMT)-mediated repair and homologous recombination repair (HR). Mechanistically, GFI1-36N exhibits impaired binding to Ndrg1 promoter element compared to GFI1-36S (wild type), causing decreased NDRG1 levels, consequently leading to suppression of MGMT expression, imprinted at the transcriptome and proteome, thus leaving the AML cells vulnerable to DNA damaging agents. Furthermore, we showed that a low expression level of GFI1 in leukemic cells is associated with high OXPHOS and enhanced glutamine metabolism. However, we hypothesise that the observed metabolic phenotype is mediated through FOXO1 protein. RNAseq transcriptomic analysis revealed higher Foxo1 mRNA expression levels with lower GFI1 expression, providing the first hint of Foxo1 as a potential target gene of GFI1 protein. The mRNA and protein levels of high Foxo1 with reduced GFI1 expression was confirmed by RT-PCR and western blot, respectively. In addition, CHIPseq and ATACseq analysis further proved that Foxo1 is a potential target gene of GFI1. In summary, we show that GFI1 plays a role during DNA repair and metabolism and thus provides critical insights into a novel therapeutic option for AML patients carrying the GFI1-36N variant or having a low expression level of GFI1.
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Project description:The zinc finger transcription factor growth-factor-independent-1 (Gfi1) has been involved in various cellular differentiation processes. Gfi1 acts as a transcriptional repressor and splicing control factor upon binding to cognate binding sites in regulatory elements of its target genes. Here, we report that Gfi1-deficient mice develop autoimmunity. Gfi1-deficient peripheral B-cells show a hyperproliferative phenotype, leading to expansion of plasma cells, increased levels of nuclear autoantibodies, and immunoglobulin deposition in brain and kidneys. Dysregulation of multiple transcription factors and cell-cycle control elements may contribute to B-cell dependent autoimmunity. Gfi1 thus emerges as a novel master-regulator restricting autoimmunity. Experiment Overall Design: Splenic B220+CD19+ CD138- B cells of 4 week old Gfi1+/+ and Gfi1-/- mice were isolated and RNA was extracted from one sample per group and microarray analysis was performed.
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