|Title||Analysis of autophagic flux in response to sulforaphane in metastatic prostate cancer cells.|
|Publication Type||Journal Article|
|Year of Publication||2015|
|Authors||Watson GW, Wickramasekara S, Fang Y, Palomera-Sanchez Z, Maier CS, Williams DE, Dashwood RH, Perez VI, Ho E|
|Journal||Mol Nutr Food Res|
|Date Published||2015 Oct|
|Keywords||Apoptosis, Autophagy, Cell Death, Cell Line, Tumor, Dose-Response Relationship, Drug, Humans, Isothiocyanates, Male, Prostatic Neoplasms|
SCOPE: The phytochemical sulforaphane (SF) has been shown to decrease prostate cancer metastases in a genetic mouse model of prostate carcinogenesis, though the mechanism of action is not fully known. SF has been reported to stimulate autophagy, and modulation of autophagy has been proposed to influence SF cytotoxicity; however, no conclusions about autophagy can be drawn without assessing autophagic flux, which has not been characterized in prostate cancer cells following SF treatment.
METHODS AND RESULTS: We conducted an investigation to assess the impact of SF on autophagic flux in two metastatic prostate cancer cell lines at a concentration shown to decrease metastasis in vivo. Autophagic flux was assessed by multiple autophagy related proteins and substrates. We found that SF can stimulate autophagic flux and cell death only at high concentrations, above what has been observed in vivo.
CONCLUSION: These results suggest that SF does not directly stimulate autophagy or cell death in metastatic prostate cancer cells under physiologically relevant conditions, but instead supports the involvement of in vivo factors as important effectors of SF-mediated prostate cancer suppression.
|Alternate Journal||Mol Nutr Food Res|
|PubMed Central ID||PMC4651621|
|Grant List||P01 CA090890 / CA / NCI NIH HHS / United States |
P30 ES000210 / ES / NIEHS NIH HHS / United States
1S10RR107903-01 / RR / NCRR NIH HHS / United States
CA090890 / CA / NCI NIH HHS / United States