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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

ABSTRACT: Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

PROVIDER: PRJNA1193517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31585644_1.fastq.gz	Fastqsanger.gz
	SRR31585644_2.fastq.gz	Fastqsanger.gz
	SRR31585645_1.fastq.gz	Fastqsanger.gz
	SRR31585645_2.fastq.gz	Fastqsanger.gz
	SRR31585646_1.fastq.gz	Fastqsanger.gz

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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

Project description:We analyzed the transcriptome changes of the colon carcinoma cell line HCT116 TP53-/- in response to expression of the TP63 isoforms deltaNp63alpha or deltaNp63beta. The goal was to understand how these C-terminal isoforms of p63 might differentially regulate gene expression.

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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

Project description:Our goal was to assess transcriptional changes of the colon carcinoma cell line HCT116 TP53-/- in response to expression of the TP63 isoforms deltaNp63alpha or deltaNp63beta. The goal was to understand how these C-terminal isoforms of p63 might differentially regulate gene expression. We also assessed how differential binding of these isoforms and how they affect local changes in H3K27ac.

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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

Project description:Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

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Project description:Purpose: To identify TP63 expression regulated pathways in HNSCC Methods: A recombinant lentivirus encoding either NS shRNA or TP63 shRNA was introduced into a HNSCC cell line, FaDu. SCCs were gene generated by implanting either FaDu-NS shRNA (n=3) or FaDu-TP63 shRNA into the tongue of athymic nude mice. Tongue SCCs harvested at the end of study were used for transcriptome analysis

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Co-expression analysis reveals gene cluster associated with methylation of enhancers and chromosomal instability under TP63 and TRIM29 regulation.

Project description:Prostate adenocarcinoma (PRAD) is the second most common cause of cancer-related deaths in men. In PRAD, high variability in DNA methylation and a high rate of large genomic rearrangements is often observed. To elucidate the reasons behind such high variance, we integrated DNA methylation, RNA-seq, and copy number alterations datasets from The Cancer Genome Atlas (TCGA) focusing on PRAD and subsequently employed weighted gene co-expression network analysis (WGCNA). Our results show that only a single cluster of co-expressed genes is associated with genomic and epigenomic instability. Within this cluster, TP63 and TRIM29 are key transcription regulators and are downregulated in PRAD. We revealed that TP63 regulates the level of enhancer methylation in prostate basal epithelium cells. TRIM29 forms a complex with TP63 and together regulate the expression of genes specific to the prostate basal epithelium. Moreover, TRIM29 binds DNA repair proteins and prevents formation of the TMPRSS2:ERG gene fusion typically observed in PRAD. Therefore, the study shows that TRIM29 and TP63 are important regulators maintaining the identity of the basal epithelium under physiological conditions. Finally, we uncover the role of TRIM29 in PRAD development.

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