7. Conclusions
We have summarised that ERα exhibits proliferative action, whereas ERβ plays an anti-proliferative role in CRPC. The majority of the researchers suggested that the castration resistance mechanisms are mainly AR-dependent pathways. However, other mechanisms, such as ADT-induced senescence, the alternative pathway of steroidogenesis, and the ER signaling pathway, are also involved in CRPC development. A deeper knowledge of the resistance mechanisms behind successive transitions from PCa to more advanced stages after ADT is necessary for the development of effective treatments for CRPC. Furthermore, our findings lay the groundwork for further research into the involvement of ERα and ERβ in PCa that results in its castration stage, CRPC, and emphasises the significance of ER distribution in various study models. Co-targeting these receptors for CRPC prevention via the modification of SERM and antioxidants is crucial to improving future therapeutic approaches.