Glucocorticoid promotes metastasis of colorectal cancer via co-regulation of glucocorticoid receptor and TET2 (ChIP-Seq)
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ABSTRACT:
PROVIDER: PRJNA1084827 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28247348_1.fastq.gz | Fastqsanger.gz | |||
| SRR28247348_2.fastq.gz | Fastqsanger.gz | |||
| SRR28247349_1.fastq.gz | Fastqsanger.gz | |||
| SRR28247349_2.fastq.gz | Fastqsanger.gz | |||
| SRR28247350_1.fastq.gz | Fastqsanger.gz |
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Project description:Background Glucocorticoids (GCs), commonly used for anti-inflammatory and cancer treatments, have been linked to the promotion of cancer metastasis. Yet, the molecular mechanisms behind this potential remain poorly understood. Clarifying these mechanisms is crucial for a nuanced understanding and potential refinement of GC therapies in the context of cancer treatment. Methods In HEK293T cells, co-immunoprecipitation (Co-IP) and chromatin immunoprecipation sequencing (ChIP-seq) were used with antibodies of GR and TET family proteins (TET1, TET2, TET3). Drup repositioning was performed through the LINCS database, using common genes of GR and TET2 in HEK293 and HCT116 cell lines with CRC differentially expressed genes (DEGs). Cell migration and invasion were tested in colorectal cancer (CRC) cell lines with varying glucocorticoid receptor (GR) expression, i.e., HCT116 and HT29 cell lines. Findings Dexamethasone (Dex) treatment resulted in a significant difference in cell migration rates in two CRC cell lines with disparate GR expression levels. Co-IP and ChIP-seq analyses substantiated the interaction between GR and TET family proteins in HEK293T cells. Belinostat, the selected compound, was successfully validated for its potential to counteract the effects of GC-induced inversion in CRC cells in vitro. Transcriptomic analyses of Belinostat-treated HCT116 cells revealed down-regulation of target genes associated with cancer metastasis.. Interpretation This study provides valuable insights into the molecular mechanisms underlying GC-induced metastasis, introducing newly repositioned compounds that could serve as potential adjuvant therapy to GC treatment. Furthermore, it opens avenues for exploring novel drug candidates for CRC treatment.
2024-06-01 | GSE261016 | GEO
Project description:Background Glucocorticoids (GCs), commonly used for anti-inflammatory and cancer treatments, have been linked to the promotion of cancer metastasis. Yet, the molecular mechanisms behind this potential remain poorly understood. Clarifying these mechanisms is crucial for a nuanced understanding and potential refinement of GC therapies in the context of cancer treatment. Methods In HEK293T cells, co-immunoprecipitation (Co-IP) and chromatin immunoprecipation sequencing (ChIP-seq) were used with antibodies of GR and TET family proteins (TET1, TET2, TET3). Drup repositioning was performed through the LINCS database, using common genes of GR and TET2 in HEK293 and HCT116 cell lines with CRC differentially expressed genes (DEGs). Cell migration and invasion were tested in colorectal cancer (CRC) cell lines with varying glucocorticoid receptor (GR) expression, i.e., HCT116 and HT29 cell lines. Findings Dexamethasone (Dex) treatment resulted in a significant difference in cell migration rates in two CRC cell lines with disparate GR expression levels. Co-IP and ChIP-seq analyses substantiated the interaction between GR and TET family proteins in HEK293T cells. Belinostat, the selected compound, was successfully validated for its potential to counteract the effects of GC-induced inversion in CRC cells in vitro. Transcriptomic analyses of Belinostat-treated HCT116 cells revealed down-regulation of target genes associated with cancer metastasis.. Interpretation This study provides valuable insights into the molecular mechanisms underlying GC-induced metastasis, introducing newly repositioned compounds that could serve as potential adjuvant therapy to GC treatment. Furthermore, it opens avenues for exploring novel drug candidates for CRC treatment.
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Project description:Glucocorticoid promotes metastasis of colorectal cancer via co-regulation of glucocorticoid receptor and TET2 (RNA-Seq)
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Project description:The glucocorticoid receptor (GR) and ten-eleven translocation 2 (TET2) respectively play a crucial role in regulating immunity and inflammation, and GR interacts with TET2. However, their syn-ergetic roles in inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), remain unclear. This study aimed to investigate the co-target gene signatures of GR and TET2 in IBD and provide potential therapeutic interventions for IBD. By integrating public data, we identified 179 GR- and TET2-targeted differentially expressed genes (DEGs) in CD and 401 in UC. These genes were closely associated with immunometabolism, inflammatory responses, and cell stress pathways. In vitro inflammatory cellular models were constructed using LPS-treated HT29 and HCT116 cells, respectively. Drug repositioning based on the co-target gene signatures of GR and TET2 derived from transcriptomic data of UC, CD, and the in vitro model were performed using the Connectivity Map (CMap). BMS-536924 emerged as a top therapeutic candidate, and its validation experiment within the in vitro inflammatory model confirmed its ef-ficacy in mitigating the LPS-induced inflammatory response. This study sheds light on the path-ogenesis of IBD from a new perspective and may accelerate the development of novel therapeutic agents for inflammatory diseases including IBD.
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