1,25(OH) 2 D 3 induced vitamin D receptor signaling negatively regulates endoplasmic reticulum-associated degradation (ERAD) and androgen receptor signaling in human prostate cancer cells.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory study using human cancer cell lines and molecular docking (bench research).
PubMed 36567009 · doi:10.1016/j.cellsig.2022.110577
What was done
Researchers investigated the molecular effects of 1,25(OH)2D3 on endoplasmic reticulum-associated degradation (ERAD), unfolded protein response (UPR) pathways (IRE1⍚ and PERK branches), and androgen receptor signaling using LNCaP and 22Rv1 human prostate cancer cell lines. They also performed molecular docking for androgen receptor signaling, examined c-Myc expression and epithelial-mesenchymal transition (EMT) markers, and tested 3D-tumor formation in LNCaP cells.
What was found
No numerical values, p-values, or effect sizes are reported in the abstract. Directionally, 1,25(OH)2D3 negatively regulated ERAD component expression, divergently controlled IRE1⍚ and PERK branches of the UPR in LNCaP and 22Rv1 cells, and inhibited androgen receptor signaling. VDR signaling also decreased c-Myc expression, reduced EMT, and significantly inhibited 3D-tumor formation of LNCaP cells.
Why it matters
The study outlines potential molecular mechanisms linking active vitamin D signaling to the suppression of androgen receptor activity and proteostasis pathways in prostate cancer models.
Limits
Findings are strictly based on in vitro cell line models and computational docking without in vivo animal or human clinical data. The abstract provides no quantitative data, sample sizes, or variance estimates.
Cited by
- supports Vitamin D functions as a hormone and influences androgen receptor activity.