TY - JOUR
T1 - Action mechanism and signal pathways of psidium guajava L. aqueous extract in killing prostate cancer LNCaP cells
AU - Chen, Kuan Chou
AU - Peng, Chiung Chi
AU - Chiu, Wen Ta
AU - Cheng, Yu Ting
AU - Huang, Guan Ta
AU - Hsieh, Chiu Lan
AU - Peng, Robert Y.
N1 - Funding Information:
The authors are grateful to the financial support from NSC-96-2320-B-241-006-MY3 and 94TMU-TMUH-02. The authors also acknowledge the partial financial supports of the grants: SKH-TMU-93-37 from the Shin Kong Wu Ho-Su Memorial Hospital and TMU96-AE1-B08 from the Taipei Medical University, Taiwan.
PY - 2010/2
Y1 - 2010/2
N2 - Aqueous extract of Psidium guajava L. budding leaves (PE) has been shown to possess anti-prostate cancer activity in a cell line model. We examined whether its bioactivity could be conserved either in the presence or the absence of synthetic androgen R1881. In both cases, PE was shown to inhibit LNCaP cell proliferation and down-regulate expressions of androgen receptor (AR) and prostate specific antigen (PSA). The cytotoxicity of PE was shown by enhanced LDH release in LNCaP cells. The flow cytometry analysis revealed cell cycle arrests at G0/G1 phase with huge amount of apoptotic LNCaP cells after treatment with PE for 48 h in a dose-responsive manner, which was also confirmed by TUNEL assay. From the results of decreased Bcl-2/Bax ratio, inactivation of phosphor-Akt, activation of phosphor-p38, phospho-Erk1/phospho- Erk2, the molecular action mechanism of PE to induce apoptosis in LNCaP cells was elucidated. Compatible with the in vitro study findings, treatment with PE (1.5 mg/mouse/day) significantly diminished both the PSA serum levels and tumor size in a xenograft mouse tumor model. Conclusively, PE is a promising anti-androgen-sensative prostate cancer agent.
AB - Aqueous extract of Psidium guajava L. budding leaves (PE) has been shown to possess anti-prostate cancer activity in a cell line model. We examined whether its bioactivity could be conserved either in the presence or the absence of synthetic androgen R1881. In both cases, PE was shown to inhibit LNCaP cell proliferation and down-regulate expressions of androgen receptor (AR) and prostate specific antigen (PSA). The cytotoxicity of PE was shown by enhanced LDH release in LNCaP cells. The flow cytometry analysis revealed cell cycle arrests at G0/G1 phase with huge amount of apoptotic LNCaP cells after treatment with PE for 48 h in a dose-responsive manner, which was also confirmed by TUNEL assay. From the results of decreased Bcl-2/Bax ratio, inactivation of phosphor-Akt, activation of phosphor-p38, phospho-Erk1/phospho- Erk2, the molecular action mechanism of PE to induce apoptosis in LNCaP cells was elucidated. Compatible with the in vitro study findings, treatment with PE (1.5 mg/mouse/day) significantly diminished both the PSA serum levels and tumor size in a xenograft mouse tumor model. Conclusively, PE is a promising anti-androgen-sensative prostate cancer agent.
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U2 - 10.1080/01635580903407130
DO - 10.1080/01635580903407130
M3 - Article
C2 - 20099201
AN - SCOPUS:76749137291
SN - 0163-5581
VL - 62
SP - 260
EP - 270
JO - Nutrition and Cancer
JF - Nutrition and Cancer
IS - 2
ER -
