Atractylenolide II Induces Apoptosis of Prostate Cancer Cells through Regulation of AR and JAK2/STAT3 Signaling Pathways.
Jing WangNasser Moussa IdeSalah AdlatMing Ming JiangNan JiangLi GaoPublished in: Molecules (Basel, Switzerland) (2018)
Prostate cancer is the most common illness affecting men worldwide. Although much progress has been made in the study of prostate cancer prevention and treatment, less attention has been paid to the molecular mechanism of the disease. The molecular arrangement by which atractylenolide II (ATR II) induces human prostate cancer cytotoxicity was comprehensively examined in the present study. As indicated by the results, ATR II could inhibit prostate cancer cell proliferation and promote DU145 and LNCaP cell apoptosis through induced G2/M cell cycle arrest. The cell apoptosis process induced by ATR II in both DU145 and LNCaP cells was associated with its ability to inhibit androgen receptor (AR) with overexpression of protein inhibitor of activated STAT-1 (PIAS1) and the repression of Janus kinase (Jak2) signaling pathways. The data from the present study demonstrated the antitumor effects and the potential pharmacological application of ATR II as an efficient drug for prostate cancer treatment.
Keyphrases
- prostate cancer
- cell proliferation
- cell cycle arrest
- radical prostatectomy
- pi k akt
- signaling pathway
- induced apoptosis
- cell death
- emergency department
- endothelial cells
- dna damage response
- transcription factor
- dna damage
- oxidative stress
- tyrosine kinase
- climate change
- binding protein
- smoking cessation
- combination therapy