Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α 2 β 1 expression.
Huai-Ching TaiShih-Wei WangSanskruti SwainLiang-Wei LinHsiao-Chi TsaiShan-Chi LiuHsi-Chin WuJeng-Hung GuoChun-Lin LiuYu-Wei LaiTien-Huang LinChiao-Wen LinChih-Hsin TangPublished in: Journal of pineal research (2022)
Advanced prostate cancer often develops into bone metastasis, which is characterized by aberrant bone formation with chronic pain and lower chances of survival. No treatment exists as yet for osteoblastic bone metastasis in prostate cancer. The indolamine melatonin (N-acetyl-5-methoxytryptamine) is a major regulator of the circadian rhythm. Melatonin has shown antiproliferative and antimetastatic activities but has not yet been shown to be active in osteoblastic bone lesions of prostate cancer. Our study investigations reveal that melatonin concentration-dependently decreases the migratory and invasive abilities of two osteoblastic prostate cancer cell lines by inhibiting FAK, c-Src, and NF-κB transcriptional activity via the melatonin MT 1 receptor, which effectively inhibits integrin α 2 β 1 expression. Melatonin therapy appears to offer therapeutic possibilities for reducing osteoblastic bone lesions in prostate cancer.
Keyphrases
- prostate cancer
- radical prostatectomy
- chronic pain
- signaling pathway
- bone mineral density
- vascular smooth muscle cells
- poor prognosis
- bone loss
- squamous cell carcinoma
- small cell lung cancer
- stem cells
- binding protein
- postmenopausal women
- risk assessment
- young adults
- genome wide
- climate change
- atrial fibrillation
- long non coding rna
- pain management
- dna methylation
- heart rate
- benign prostatic hyperplasia
- human health