Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.

Epithelial-mesenchymal transition (EMT) is a dynamic process of lineage plasticity in which epithelial cancer cells acquire mesenchymal traits, enabling them to metastasize to distant organs. This review explores the current understanding of how lineage plasticity and phenotypic reprogramming drive prostate cancer progression to lethal stages, contribute to therapeutic resistance, and highlight strategies to overcome the EMT phenotype within the prostate tumor microenvironment (TME). Emerging evidence reveals that prostate tumor cells can undergo lineage switching, adopting alternative growth pathways in response to anti-androgen therapies and taxane-based chemotherapy. These adaptive mechanisms support tumor survival and growth, underscoring the need for deeper insights into the processes driving prostate cancer differentiation, including neuroendocrine differentiation and lineage plasticity. A comprehensive understanding of these mechanisms will pave the way for innovative therapeutic strategies. Effectively targeting prostate cancer cells with heightened plasticity and therapeutic vulnerability holds promise for overcoming treatment resistance and preventing tumor recurrence. Such advancements are critical for developing effective approaches to prostate cancer treatment and improving patient survival outcomes.