Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells

Proteome Science

Research

Shudong Zhu¹  Chang-Yan Chen¹  Sun-Mi Yun²  Ji-Hyun Kim²  Chan-Hee Lee²  Sung-Hoon Kim²  Kyoo-Seok Ahn²  Soo-Jin Jeong²  Suk-Hyun Won²  Hyo-Jeong Lee²  Kwang Seok Ahn²  Hyo-Jung Lee²  Hyun Seok Kim³ 

[1] Beth Israel Deaconess Medical Center, Harvard Medical School, 02215, Boston, MA, USA;College of Oriental Medicine, Kyung Hee University, 130-701, Seoul, Republic of Korea;Yonsei University School of Medicine, 120-752, Seoul, South Korea;

关键词: Sodium Dodecyl Sulphate;    Protein Spot;    Activin;    LNCaP Cell;    TUNEL Assay;   

DOI  :  10.1186/1477-5956-8-67

 received in 2010-08-10, accepted in 2010-12-16,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundSulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables that exerts anti-oxidant, anti-inflammatory, anti-cancer and radio-sensitizing activities. Nonetheless, the mechanism responsible for SFN-induced cell death is not fully understood. In the present study, anti-cancer mechanism of SFN was elucidated in LNCaP prostate cancer cells.ResultsSFN exerted cytotoxicity and increased TUNEL positive cells in a concentration-dependent manner in LNCaP cells. Proteomics study revealed that levels of nine proteins including tubulin β-2, phosphoglucomutase-3 (PGM3), melanoma-derived leucine zipper containing extra-nuclear factor, activin A type I receptor precursor, smoothelin-A, KIA0073, hypothetical protein LOC57691 and two unnamed proteins were changed over 8 folds in SFN treated LNCaP cells compared to untreated control. We have further confirmed that SFN reduced PGM3 expression with western blotting and showed that PGM3 siRNA enhanced cytotoxicity demonstrated by cell morphology and TUNEL assays in LNCaP cells.ConclusionTaken together, these findings suggest that PGM3 plays a role in mediating SFN-induced cell death in LNCaP cells, and is a potential molecular therapeutic target for prostate cancer.

【 授权许可】

Unknown   
© Lee et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.