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A Transcriptome-wise Atlas of Human Prostate as a Function of Postmortem Interval Time

ABSTRACT: The prostate gland is one of the last internal organs to deteriorate during human decomposition. However, the effect of postmortem interval (PMI) on the mRNA and lncRNA expression and splicing is yet to be investigated in detail. The current study aims to identify the functional role of postmortem gene induction and pathway activation in prostate tissues with respect to the PMI gradient. The cadaver samples that were used in this study were collected during forensic autopsies and preserved at -20°C within the morgue at the University of Pavia (Pavia, Italy). After RNA extraction, total RNA sequencing was performed on Illumina’s NovaSeq 6000 using paired-ended sequencing approach. StringTie was used to perform expression level for mRNAs and lncRNAs by calculating FPKM. Additionally, mRNAs/lncRNAs differential expression analysis was performed by DESeq2. rMATS (version 4.1.1) was used to identify alternative splicing events and analyze differential alternative splicing events between samples having high and low PMI. Pathway analysis of the differentially expressed genes demonstrated the enrichment of FoxO signaling, aldosterone-regulated sodium reabsorption and adipocytokine signaling pathways in prostate tissue with high PMI. Gene Set Enrichment Analysis (GSEA) indicated the positive enrichment of genes belonging from protein export, proteasome, ferroptosis, and citric acid cycle in high PMI group. A comprehensive detection of alternative splicing events (ASEs) at the cellular level in postmortem prostate tissue was performed to reveal skipped exon events to be most prominent ASE in high PMI group followed by retained intron events. Our study implies that the transcription machinery remains active in prostate tissue even after five days postmortem.

ORGANISM(S): Homo sapiens

PROVIDER: GSE291070 | GEO | 2026/01/14

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE291070_4_genes_fpkm_expression.xlsx	Xlsx
	GSE291070_5_isoforms_fpkm_expression.xlsx	Xlsx
	GSE291070_gene_count_matrix.xlsx	Xlsx
	GSE291070_transcript_count_matrix.xlsx	Xlsx

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Project description:Rationale: Prostate cancer is one of the most common malignant tumors occurring in the male reproductive system. Androgen deprivation therapy (ADT) is the primary treatment for prostate cancer. However, approximately 10% to 20% of advanced prostate cancer patients progress to castration-resistant prostate cancer (CRPC) within five years, posing a significant challenge to treatment. There is an urgent need to explore the causes and mechanisms of prostate cancer progression, and to identify new therapeutic targets and predictive markers.Methods: Utilize RNA-seq to screen for differentially expressed genes and alternative splicing events between androgen-sensitive prostate cancer cells and castration-resistant prostate cancer cells. Perform bioinformatics analysis on the differentially expressed genes. The expression levels of these genes were confirmed by real-time quantitative PCR (RT-qPCR); alternative splicing events related to castration resistance were verified through RT-PCR. The impact of the S100A6 gene on the proliferation and growth capabilities of PC3 and DU145 cells was analyzed using CCK8, colony formation, and EdU assays. Cell migration was assessed using a wound healing assay.Results: The RNA-seq analysis results showed that there were 4,830 differentially expressed genes in non-hormone-sensitive prostate cancer. GO and KEGG enrichment analysis of these differentially expressed genes revealed significant enrichment in tumor-related signaling pathways such as regulation of cell cycle process, cell division, and regulation of cell projection organization. Further RT-qPCR detection results indicated that the mRNA expression of four genes, including S100A6, was upregulated, consistent with the transcriptome sequencing results. Downregulation of S100A6 expression significantly inhibited the proliferation and migration of non-hormone-dependent prostate cancer. In this study, we also identified many splicing alterations in cancer-related genes, with castration resistance-induced alternative splicing events closely related to the interaction networks of regulation of cell cycle process, cell division, and regulation of cell projection organization.Conclusions: Our research findings suggest that S100A6 may serve as a molecular marker or therapeutic target associated with castration resistance in prostate cancer, providing new insights into the molecular basis of this disease.

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A Transcriptome-wise Atlas of Human Prostate as a Function of Postmortem Interval Time

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