Baicalein inhibits prostate cancer cell growth and metastasis via the caveolin-1/AKT/mTOR pathway

• Published in: Molecular and cellular biochemistry Vol. 406; no. 1-2; pp. 111 - 119
• Main Authors: Guo, Zhaoxin, Hu, Xiaolin, Xing, Zhaoquan, Xing, Rui, Lv, Renguang, Cheng, Xiangyu, Su, Jing, Zhou, Zunlin, Xu, Zhonghua, Nilsson, Sten, Liu, Zhaoxu
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.08.2015; Springer; Springer Nature B.V
• Subjects: Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Biochemistry; Biomedical and Life Sciences; Cancer metastasis; Cardiology; Caveolin 1 - metabolism; Cell growth; Cell Movement; Cell Proliferation - drug effects; Drug Screening Assays, Antitumor; Flavanones - pharmacology; Flavonoids; Growth; Health aspects; Health risks; Humans; Isoflavones; Life Sciences; Male; Medical Biochemistry; Medicin och hälsovetenskap; Metastasis; Neoplasm Metastasis; Oncology; Prostate cancer; Prostatic Neoplasms - drug therapy; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Proto-Oncogene Proteins c-akt - metabolism; Signal Transduction - drug effects; TOR Serine-Threonine Kinases - metabolism; Caveolin-1; Baicalein; Androgen-independent prostate cancer; Metastasis; Anti-cancer activity
• ISSN: 0300-8177; 1573-4919; 1573-4919
• DOI: 10.1007/s11010-015-2429-8

Prostate cancer (PCa) is lethal type of genitourinary cancer due to its high morbidity and gradual resistance to androgen deprivation therapy. Accumulating evidence has recently suggested that the daily intake of flavonoids is negatively correlated with the risk of cancer. In this study, we aimed to investigate the potential effects of baicalein on androgen-independent PCa cells and the underlying mechanisms through which baicalein exerts its actions. Cell viability and flow cytometric apoptosis assays indicated that baicalein potently suppressed the growth and induced the apoptosis of DU145 and PC-3 cells in a time- and dose-dependent manner. Consistently, the inhibitory effects of baicalein on migration and invasion were also observed in vitro. Mechanistically, we found that baicalein can suppress caveolin-1 and the phosphorylation of AKT and mTOR in a time- and dose-dependent manner. Moreover, the inhibition of the activation of AKT with LY294002 significantly promoted the apoptosis and metastasis induced by baicalein. In conclusion, these findings suggested that baicalein can induce apoptosis and inhibit metastasis of androgen-independent PCa cells through inhibition of the caveolin-1/AKT/mTOR pathway, which implies that baicalein may be a potential therapeutic agent for the treatment of androgen-independent prostate cancer patients.