Prostate cancer and metastasis: an emphasis on EMT mechanism

Metastasis from prostate cancer is still a major problem, affecting patients' mortality rates and quality of life in general. Moreover, the presence of metastases is a direct determinant of the prognosis and clinical outcome of prostate cancer. Furthermore, metastasis thrives in the bone microenvironment. The progression of androgen-sensitive to castration-resistant and metastatic prostate cancer is a major clinical concern in prostate cancer treatment. In their normal state, epithelial cells form a monolayer that is adherently held in place by proteins that inhibit cell movement. Epithelial cells in prostate cancer can change their shape from cuboidal to spindle-shaped as the disease advances; this process is called epithelial-mesenchymal transition (EMT). Despite efforts to block the androgen receptor (AR) signaling axis, the exact molecular process by which androgen independence kills is yet unknown. The involvement of cancer stem cells (CSCs) and epithelial-to-mesenchymal transition (EMT) in the progression of prostate cancer to castration-resistant and metastasis are being more and more highlighted by new findings. This EMT procedure may be evolving over time. It is worth noting that metastatic disease development in prostate tumors may trigger the reactivation of a dormant embryonic pathway known as the epithelial-mesenchymal transition (EMT). A mesenchymal phenotype resembling cancer stem cells can be achieved by malignancies by EMT.