Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells
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Published on: June 13, 2020
Chan-Hee Lee1, Soo-Jin Jeong1, Sun-Mi Yun1
1College of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
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.
Insights
Sulforaphane (SFN) induces prostate cancer cell death by altering protein levels, particularly reducing phosphoglucomutase-3 (PGM3). Lowering PGM3 enhances SFN
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Sulforaphane (SFN), a cruciferous vegetable compound, exhibits antioxidant, anti-inflammatory, anticancer, and radiosensitizing properties.
- The precise mechanism of SFN-induced cancer cell death remains incompletely understood.
- This study investigates the anti-cancer mechanism of SFN in LNCaP prostate cancer cells.
Purpose of the Study:
- To elucidate the anti-cancer mechanism of sulforaphane (SFN) in LNCaP prostate cancer cells.
- To identify proteins affected by SFN treatment and their role in cell death.
- To evaluate phosphoglucomutase-3 (PGM3) as a potential therapeutic target.
Main Methods:
- Proteomic analysis to identify proteins altered by SFN treatment in LNCaP cells.
- Western blotting to confirm changes in specific protein expression (PGM3).
- RNA interference (siRNA) to reduce PGM3 expression and assess its impact on cytotoxicity.
- TUNEL assays and cell morphology analysis to quantify cell death.
Main Results:
- SFN treatment resulted in concentration-dependent cytotoxicity and increased TUNEL-positive LNCaP cells.
- Proteomics identified nine proteins, including phosphoglucomutase-3 (PGM3), with significant expression changes (over 8-fold) upon SFN treatment.
- SFN reduced PGM3 expression, and PGM3 siRNA enhanced SFN-induced cytotoxicity, as evidenced by cell morphology and TUNEL assays.
Conclusions:
- Phosphoglucomutase-3 (PGM3) plays a significant role in mediating sulforaphane (SFN)-induced cell death in LNCaP prostate cancer cells.
- PGM3 represents a potential molecular therapeutic target for prostate cancer treatment.
- These findings contribute to understanding SFN's anti-cancer mechanisms and developing targeted therapies.
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