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Open AccessArticle

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

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, Heilongjiang, China
College of Animal Science, Heilongjiang Agriculture Economics Vocational College, Mudanjiang 157041, Heilongjiang, China
Colleges of Life Science and Technology, Dalian University, Dalian Economical Technological Development Zone, Dalian 116622, Liaoning, China
Author to whom correspondence should be addressed.
Molecules 2018, 23(12), 3298;
Received: 4 November 2018 / Revised: 3 December 2018 / Accepted: 6 December 2018 / Published: 12 December 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. View Full-Text
Keywords: ATR II; JAK2/STAT3; apoptosis; G2/M arrest; AR/PIAS1 ATR II; JAK2/STAT3; apoptosis; G2/M arrest; AR/PIAS1
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Wang, J.; Nasser, M.I.; Adlat, S.; Ming Jiang, M.; Jiang, N.; Gao, L. Atractylenolide II Induces Apoptosis of Prostate Cancer Cells through Regulation of AR and JAK2/STAT3 Signaling Pathways. Molecules 2018, 23, 3298.

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