GATA4 and GATA6 loss-of-expression is associated with extinction of the "classical" programme and poor outcome in pancreatic ductal adenocarcinoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA860210 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20318431_1.fastq.gz | Fastqsanger.gz | |||
| SRR20318431_2.fastq.gz | Fastqsanger.gz | |||
| SRR20318432_1.fastq.gz | Fastqsanger.gz | |||
| SRR20318432_2.fastq.gz | Fastqsanger.gz | |||
| SRR20318433_1.fastq.gz | Fastqsanger.gz |
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Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.
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Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes.
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Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. ChIP-Seq experiments of KLF5, GATA4 and GATA6 were performed in three gastric cancer cell lines YCC3, AGS and KATOIII
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