Transcriptome data analyses of prostatic hyperplasia in Esr2 knockout rats

Area of Science:

• Endocrinology
• Molecular Biology
• Urology

Background:

• Estrogen signaling is crucial in prostate pathophysiology.
• Estrogen receptor alpha (ESR1) promotes stromal cell proliferation.
• Estrogen receptor beta (ESR2) inhibits glandular epithelial proliferation and promotes differentiation.

Purpose of the Study:

• To identify ESR2-target genes in the rat prostate.
• To elucidate molecular mechanisms underlying ESR2's role in prostate homeostasis.
• To investigate the impact of ESR2 disruption on gene expression.

Main Methods:

• RNA-sequencing (RNA-seq) was performed on prostate glands from wildtype and Esr2 knockout (Esr2-/-) rats.
• High-quality RNA-seq reads were aligned to the Rattus norvegicus genome.
• Differential gene expression analysis identified significant changes (fold change ≥ 2, p-value ≤ 0.05).

Main Results:

• Out of 32,623 detected genes, 824 were differentially expressed in Esr2-/- prostates.
• 550 genes were downregulated and 274 genes were upregulated in the absence of ESR2.
• Pathway analysis indicated altered gene expression related to epithelial proliferation and benign tumor formation.

Conclusions:

• Disruption of ESR2 signaling in rats leads to prostatic glandular hyperplasia.
• RNA-seq analysis identified numerous differentially expressed genes in Esr2-/- prostates.
• Altered gene expression pathways are linked to prostate epithelial proliferation and tumorigenesis, highlighting ESR2's critical role.