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

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

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Title: Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells
Author: Lee, Chan-Hee; Jeong, Soo-Jin; Yun, Sun-Mi; Kim, Ji-Hyun; Lee, Hyo-Jung; Ahn, Kwang Seok; Won, Suk-Hyun; Lee, Hyo-Jeong; Ahn, Kyoo-Seok; Kim, Sung-Hoon; Kim, Hyun Seok; Zhu, Shudong; Chen, Chang-Yan

Note: Order does not necessarily reflect citation order of authors.

Citation: Lee, Chan-Hee, Soo-Jin Jeong, Sun-Mi Yun, Ji-Hyun Kim, Hyo-Jung Lee, Kwang Seok Ahn, Suk-Hyun Won, et al. 2010. Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells. Proteome Science 8: 67.
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Abstract: Background: Sulforaphane (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. Results: SFN 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. Conclusion: Taken 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.
Published Version: doi:10.1186/1477-5956-8-67
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024296/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4878924

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