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Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

ABSTRACT: Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

PROVIDER: PRJNA748989 | ENA |

REPOSITORIES: ENA

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Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

Project description:Isoginkgetin (IGG) is a small molecule inhibitor of the spliceosome although the direct target remains elusive. Widespread failure to accurately remove introns poses a risk to cells and organisms through the potential production of aberrant mRNAs and proteins. The cellular responses to accumulation of these intermediates and/or the direct interference of spliceosome assembly itself may constitute a splicing stress but this is not well defined yet. We used oligonucleotide microarrays to assess genome wide changes in gene expression associated with exposure to IGG in HCT116 cells and an isogenic subline lacking the p53 tumor suppressor that responds to a variety of transcriptional stresses (Oncogene 18 (3), 583-592). Two of the 3 enriched pathways identified using PANTHER analysis of differentially expressed transcripts are linked to the ATF4 transcription factor and these effects are p53-independent.

2021-07-23 | GSE180623 | GEO

RNA sequencing analysis of isoginkgetin and thapsigargin treated HCT116 and HCT116 ATF4 deficient cells

Project description:Activating transcription factor 4 (ATF4) is activated during cellular stress through a pathway called the integrated stress response (ISR). We had previously reported that the splicing inhibitor isoginkgetin (IGG) activates ATF4 and ATF4-dependent transcripts. To determine the role of ATF4 in the transcriptional response to IGG, we used tandem CRISPR cas9 gene editing to create an ATF4 deficient HCT116 (colon cancer) cell line. We completed RNA sequencing on HCT116 parental and HCT116 ATF4 deficient cells treated with IGG, and thapsigargin (Tg), a positive control for ATF4 activation. We found that IGG led to the differential expression of 76 transcripts, and 58 of these were dependent on ATF4. Tg led to a far more robust transcriptional response, which appeared to be less ATF4 dependent.

2024-10-09 | GSE249009 | GEO

RNA sequencing analysis of isoginkgetin and thapsigargin treated HCT116 and HCT116 ATF4 deficient cells

Project description:RNA sequencing analysis of isoginkgetin and thapsigargin treated HCT116 and HCT116 ATF4 deficient cells

| PRJNA1047008 | ENA

Microarray dataset supporting a role for ATF4 in isoginkgetin-induced gene expression in HCT116 cells.

Project description:Isoginkgetin (IGG) is a compound originally derived from the leaves of Ginkgo biloba trees. It was subsequently identified through a chemical screen to be an inhibitor of both the major and minor spliceosome, with an IC50 value of 30 µM [1]. Little is currently known about the overall effects of spliceosome inhibition on human cells. Here, we treated HCT116 and a p53 null subline of colon cancer cells with 30 µM IGG for 8 hours. Total RNA was isolated, and Affymetrix oligonucleotide microarray analysis was completed using samples from two biologically independent experiments. A relatively small number of transcripts were differentially expressed in these cell lines. There was considerable overlap in the upregulated but not the downregulated transcripts. PANTHER Reactome analysis of these shared upregulated transcripts identified enriched pathways involving the ATF4 transcription factor important in the integrated stress response [2].

| S-EPMC9019238 | biostudies-literature

H2O2-treated and untreated HCT116 cells

Project description:H2O2-treated and untreated HCT116 cells

| PRJNA305862 | ENA

Liver gene expression analysis of male ApoE-/- mice treated with Isoginkgetin

Project description:Liver gene expression analysis of male ApoE-/- mice treated with Isoginkgetin

| PRJNA1089219 | ENA

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [RNA-Seq]

Project description:Purpose: Our previous studies have identified Isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates gene expression in HepG2 cells. Methods: RNA-seq was performed with two repetitions in HepG2 followed by treatment with DMSO and 20 μM Isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters in HepG2 cells.

2023-03-22 | GSE188533 | GEO

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-Seq]

Project description:Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seq for H3K27ac was performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

2023-03-22 | GSE188534 | GEO

RiboMethSeq of HCT116 cells treated with siCoilin

Project description:RiboMethSeq of HCT116 cells treated with siCoilin

| PRJNA742051 | ENA

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-seq 2]

Project description:Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seqs for H3K4me, H4K8ac, H3K27me3 and H3K9ac were performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

2023-03-22 | GSE202612 | GEO

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