We explored the effects of 1,25(OH) D, an active form of vitamin D, on prostate cancer cells, particularly focusing on its ability to influence endoplasmic reticulum-associated degradation (ERAD) and androgen receptor signaling. Previous research highlighted that the vitamin D receptor (VDR) decreases in many cancer types, including prostate cancer, prompting our investigation into how vitamin D3 could be a potential ally against tumor growth.
Our findings revealed that vitamin D3 negatively impacts ERAD components, playing a role in the unfolded protein response (UPR) within LNCaP human prostate cancer cells. Interestingly, we noted a dual regulatory effect where VDR signaling inhibited androgen signaling, suggesting that it may limit the cancer's ability to progress. This was further supported by molecular docking studies indicating that vitamin D3 could effectively inhibit androgen receptor activity.
Additionally, we discovered that VDR signaling appears to impede tumor progression by lowering levels of c-Myc, a protein often associated with cancer advancement, and reducing the epithelial-mesenchymal transition (EMT). Furthermore, treatment with vitamin D3 significantly hampered the formation of three-dimensional tumor structures in LNCaP cells, hinting at its practical uses in inhibiting tumor growth.
Overall, our investigation indicates that deeper understanding of VDR signaling could open doors to enhanced therapies for various cancers, including how estrogenic signals affect breast cancer. The data suggests that vitamin D3 could provide valuable benefits in prostate cancer treatment, particularly in slowing its progression through multiple mechanisms.