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.
Thank you for posting. This is quite a long and complex article, however it does look important. One of my key takes is to do with senescence cells. That getting rid of them is a good thing. I think ex forum legend Nalkrats, hopefully he is ok, wrote a big piece on getting rid of senescence cells.
This is old news. It turns out that ER-alpha activity is almost non-existent in normal prostate epithelial cells, but is found more often the more advanced the prostate cancer is. For castrate resistent prostate cancer it is 94%.
There is no known way to reduce the amount of ER-alpha present. The best one can do is to minimize the amount of estradiol present because without estradiol, PCa with lots of ER-alpha has no selective growth advantage over PCa with no ER-alpha. The only caveat is that a little bit of estradiol is needed for optimum health.
Because PCa typically has more ER-beta than ER-alpha, estradiol (e.g. in a patch) causing an increase in the death rate of PCa. However, in theory, if estradiol is continued then natural selection will eventually cause the PCa population to have more ER-alpha than ER-beta causing a decrease in the death rate of PCa. Because we are talking about random mutations, there is no way to determine in advance how long before ER-alpha becomes more prevalent than ER-beta.
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PTEN loss is not a determinant of time to castration-resistance following androgen-deprivation therapy in prostate cancer
Inhibition of estrogen signaling through depletion of estrogen receptor alpha by ursolic acid and betulinic acid from Prunella vulgaris var.
