Anti-proliferative effect of Cannabidiol in Prostate cancer cell PC3 is mediated by apoptotic cell death, NFκB activation, increased oxidative stress, and lower reduced glutathione status.
Jie LiTengfei GuShengping HuBaiye JinPublished in: PloS one (2023)
Prostate cancer is the second most frequent cancer diagnosed in men in the world today. Almost all prostate cancers are adenocarcinomas and develop from gland cells. We used the PC3 prostate cancer cell line, which is well studied and derived from a bone metastasis of a grade IV prostatic adenocarcinoma. Cannabidiol (CBD), a major non-psychoactive constituent of cannabis, is a cannabinoid with anti-tumor properties but its effects on prostate cancer cells are not studied in detail. Here, we found cannabidiol decreased prostate cancer cell (PC3) viability up to 37.25% and induced apoptotic cell death in a time and dose-dependent manner. We found that CBD activated the caspases 3/7 pathways and increased DNA fragmentation. Furthermore, we observed an increase of pro-apoptotic genes Bax, an increased level of reactive oxygen species, lower reduced glutathione level, and altered mitochondrial potential in response to CBD treatment leading to lower cellular ATP. Overall, our results suggest that CBD may be effective against prostate cancer cells.
Keyphrases
- cell death
- prostate cancer
- cell cycle arrest
- oxidative stress
- radical prostatectomy
- induced apoptosis
- diabetic rats
- reactive oxygen species
- benign prostatic hyperplasia
- signaling pathway
- squamous cell
- papillary thyroid
- dna damage
- endoplasmic reticulum stress
- squamous cell carcinoma
- anti inflammatory
- gene expression
- ischemia reperfusion injury
- pi k akt
- high glucose
- solid state
- immune response
- lps induced
- climate change
- young adults
- middle aged
- combination therapy
- lymph node metastasis
- nuclear factor
- cell proliferation
- drug induced
- human health
- toll like receptor
- dna methylation
- stress induced
- genome wide identification