Atractylenolide II Induces Apoptosis of Prostate Cancer Cells through Regulation of AR and JAK2/STAT3 Signaling Pathways.

Abstract

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.

• Authors: Jing Wang, Moussa Ide Nasser, Salah Adlat, Ming Ming Jiang, Nan Jiang, Li Gao
• Journal: Molecules (Basel, Switzerland) (Molecules) Vol. 23 Issue 12 (Dec 12 2018) ISSN: 1420-3049 [Electronic] Switzerland
• PMID: 30545141 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• Lactones
• Receptors, Androgen
• STAT3 Transcription Factor
• STAT3 protein, human
• Sesquiterpenes
• atractylenolide II
• JAK2 protein, human
• Janus Kinase 2

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Cell Line, Tumor
• Humans
• Janus Kinase 2 (antagonists & inhibitors, metabolism)
• Lactones (pharmacology)
• Male
• Prostatic Neoplasms (drug therapy, metabolism, pathology)
• Receptors, Androgen (metabolism)
• STAT3 Transcription Factor (antagonists & inhibitors, metabolism)
• Sesquiterpenes (pharmacology)
• Signal Transduction