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. 2009 Nov 30:9:414.
doi: 10.1186/1471-2407-9-414.

Selenium enrichment of broccoli sprout extract increases chemosensitivity and apoptosis of LNCaP prostate cancer cells

Rizky Abdulah  1 , Ahmad Faried, Kenji Kobayashi, Chiho Yamazaki, Eka W Suradji, Kazuto Ito, Kazuhiro Suzuki, Masami Murakami, Hiroyuki Kuwano, Hiroshi Koyama
Affiliations

Selenium enrichment of broccoli sprout extract increases chemosensitivity and apoptosis of LNCaP prostate cancer cells

Rizky Abdulah et al. BMC Cancer. .

Abstract

Background: Broccoli is a Brassica vegetable that is believed to possess chemopreventive properties. Selenium also shows promise as an anticancer agent. Thus, selenium enrichment of broccoli has the potential to enhance the anticancer properties of broccoli sprouts.

Method: Selenium-enriched broccoli sprouts were prepared using a sodium selenite solution. Their anticancer properties were evaluated in human prostate cancer cell lines and compared with those of a control broccoli sprout extract.

Results: Selenium-enriched broccoli sprouts were superior to normal broccoli sprouts in inhibiting cell proliferation, decreasing prostate-specific antigen secretion, and inducing apoptosis of prostate cancer cells. Furthermore, selenium-enriched broccoli sprouts but, not normal broccoli sprouts, induced a downregulation of the survival Akt/mTOR pathway.

Conclusion: Our results suggest that selenium-enriched broccoli sprouts could potentially be used as an alternative selenium source for prostate cancer prevention and therapy.

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Figures

Figure 1
Figure 1
Selenium speciation of the SeSp extract using HPLC/ICP-MS. cps: counts per second.
Figure 2
Figure 2
Effects of 24 h treatment of various CSp and SeSp concentrations to (A) LNCaP, (B) PC-3, (C) DU-145 and (D) CHEK-1 cells viability. CPI: cell proliferation inhibition.
Figure 3
Figure 3
Effects of 24 h treatment of CSp and SeSp to LNCaP cells. Cells treated with CSp regained their normal PSA secretion, cell cycle distribution, and proliferation ability after being released from the CSp treatment. (A) PSA secretion in LNCaP cells treated with CSp and SeSp extracts. PSA values were normalized against the total protein concentration of viable cells. (B) Effects of CSp and (C) SeSp extracts on the LNCaP cell cycle. Cells were harvested at indicated times and analyzed by flow cytometry. (D) Representative photomicrographs of LNCaP cells treated with CSp and (E) SeSp extracts at each IC50 concentration at various time points.
Figure 4
Figure 4
Western blot analysis of (A) upregulation of the apoptotic-related proteins and (B) downregulation of cell survival-related proteins in LNCaP cells treated with CSp or SeSp for 24 h and harvested at the indicated times. * indicates the cleaved form measured using densitometric analysis. ✮ indicates that the effects induced by CSp and SeSp are significantly different (p < 0.001, by two-way ANOVA).
Figure 5
Figure 5
Proposed schematic charts showing various mechanisms by which CSp and SeSp extracts inhibit LNCaP cell proliferation. Both extracts induced apoptosis through the extrinsic caspase-8 and intrinsic caspase-9 pathway. However, only the SeSp extract inhibited Akt phosphorylation and downstream mTOR phosphorylation, resulting in the inhibition of cell proliferation and survival.
See this image and copyright information in PMC

References

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