Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.
Level 5 - mechanism / opinion, no new human data
Narrative review describing molecular mechanisms without new human data
PubMed 39273194 · doi:10.3390/ijms25179245
What was done
This narrative review summarizes the biological roles, signaling mechanisms, and regulatory crosstalk of nuclear hormone receptors in prostate cancer, specifically examining the androgen receptor (AR), thyroid hormone receptors (TRs), retinoic acid receptors (RARs), and the vitamin D receptor (VDR).
What was found
The abstract provides qualitative mechanistic descriptions and directions of effect without numerical data: - AR ligand binding and nuclear translocation activates gene expression and supports prostate cancer proliferation. - TRs, RARs, and VDR bind chromatin as heterodimers with retinoid X receptors (RXRs) to repress basal gene expression, with ligand binding triggering transcriptional activation. - RARγ activation and 3,5,3'-triiodo-L-thyronine (T3) stimulation of TRβ promote prostate cancer cell growth. - Ligand stimulation of VDR drives growth arrest, differentiation, and apoptosis in prostate cancer cells. - Evidence indicates functional crosstalk and receptor interactions that could inform multi-receptor therapeutic strategies.
Why it matters
Understanding the interplay between androgen and non-androgen nuclear hormone receptors may provide biological targets for combinatorial regimens in prostate cancer.
Limits
The review relies on mechanistic and preclinical concepts with no quantitative data, sample sizes, or systematic review methodology reported in the abstract. Therapeutic efficacy and safety in clinical human populations were not evaluated.
Cited by
- supports Vitamin D functions as a hormone and influences androgen receptor activity.