Prostate cancer is one of the most prevalent cancers worldwide, imposing a significant burden on healthcare systems. Most cases are slow-growing; however, a minority progress to metastatic, lethal disease. Despite the relatively low mortality rate, high incidence of prostate cancer results in a substantial number of deaths.

Prognostication is primarily based on evaluating disease severity through clinical measurements, imaging, and histological evaluation. In localised prostate cancer, treatment decisions are informed by stratifying patients by the risk of disease progression. Low-risk cases are commonly managed through active surveillance, which helps avoid the morbidities associated with invasive treatments. By contrast, high-risk cases often undergo definitive local therapies, such as radical prostatectomy or radiotherapy, and adjuvant therapy. Cases presenting with intermediate-risk disease pose a more complex challenge for treatment selection. Consequently, there is a clear clinical need for additional prognostic tools for more precise differentiation between those who would benefit from invasive therapy with curative intention and those whose disease can be managed through active monitoring.

The ANO7 gene is predominantly expressed in normal prostate tissue and prostate cancer. Genomic analyses have linked ANO7 to the risk of prostate cancer and its more aggressive forms. Until recently, little was understood about the role of ANO7 in cellular physiology and pathophysiology. We found that ANO7 transcripts are enriched in the nuclei of prostatic luminal cells and prostate cancer cells, which indicates that ANO7 is subject to post-transcriptional regulation via retained introns. We report that ANO7 is highly expressed in luminal cells, but its expression is diminished in inflammation-induced club cell transformation in benign prostate glandular epithelium. We show that ANO7 is associated with both androgen receptor signalling and lipid metabolism in luminal cells, as well as the presence of CD56bright natural killer cells in the epithelium. We present evidence showing that ANO7 possibly serves a protective role and is particularly significant in low-grade cancer, where cancer-promoting lipid metabolism drives disease progression.

The results presented in this thesis bring information about the role of ANO7 in prostate cancer. Further investigations about the cellular mechanisms of ANO7 is warranted for implementation of ANO7 protein-altering germ-line mutations in clinical setting to improve risk stratification among prostate cancer patients.