SH003 induces apoptosis of DU145 prostate cancer cells by inhibiting ERK-involved pathway

BMC Complementary and Alternative Medicine

Research Article

Sung-Gook Cho¹  Yu-Jeong Choi²  Seong-Gyu Ko³  Soo-Yeon Kang⁴  Kang Min Lee⁴  Youn Kyung Choi⁵ 

[1] Department of Biotechnology, Korea National University of Transportation, 368-701, Jeungpyeong, Chungbuk, Korea;Department of Cancer Preventive Material Development, Graduate School, Kyung Hee University, 02447, Seoul, Korea;Department of Preventive Medicine, College of Korean Medicine, Kyung Hee University, 1 Hoegi, 130-701, Seoul, Korea;Department of Science in Korean Medicine, Graduate School, Kyung Hee University, 02447, Seoul, Korea;Jeju International Marine Science center for Research & Education, Korea Institute of Ocean Science & Technology (KIOST), 63349, Jeju, Korea;

关键词: SH003;    Herbal medicine;    Apoptosis;    ERK pathway;    DU145 human prostate cancer cells;    Anticancer effect;   

DOI  :  10.1186/s12906-016-1490-5

 received in 2016-07-27, accepted in 2016-11-17,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundHerbal medicines have been used in cancer treatment, with many exhibiting favorable side effect and toxicity profiles compared with conventional chemotherapeutic agents. SH003 is a novel extract from Astragalus membranaceus, Angelica gigas, and Trichosanthes Kirilowii Maximowicz combined at a 1:1:1 ratio that impairs the growth of breast cancer cells. This study investigates anti-cancer effects of SH003 in prostate cancer cells.MethodsSH003 extract in 30% ethanol was used to treat the prostate cancer cell lines DU145, LNCaP, and PC-3. Cell viability was determined by MTT and BrdU incorporation assays. Next, apoptotic cell death was determined by Annexin V and 7-AAD double staining methods. Western blotting was conducted to measure protein expression levels of components of cell death and signaling pathways. Intracellular reactive oxygen species (ROS) levels were measured using H2DCF-DA. Plasmid-mediated ERK2 overexpression in DU145 cells was used to examine the effect of rescuing ERK2 function. Results were analyzed using the Student’s t-test and P-values < 0.05 were considered to indicate statistically-significant differences.ResultsOur data demonstrate that SH003 induced apoptosis in DU145 prostate cancer cells by inhibiting ERK signaling. SH003 induced apoptosis of prostate cancer cells in dose-dependent manner, which was independent of androgen dependency. SH003 also increased intracellular ROS levels but this is not associated with its pro-apoptotic effects. SH003 inhibited phosphorylation of Ras/Raf1/MEK/ERK/p90RSK in androgen-independent DU145 cells, but not androgen-dependent LNCaP and PC-3 cells. Moreover, ERK2 overexpression rescued SH003-induced apoptosis in DU145 cells.ConclusionsSH003 induces apoptotic cell death of DU145 prostate cancer cells by inhibiting ERK2-mediated signaling.

【 授权许可】

CC BY   
© The Author(s). 2016