These results indicate that resveratrol can activate apoptotic pathways in uterine cancer cells.
COX activity might not be involved in resveratrol-induced cell proliferation
High-dose of resveratroltriggered apoptosis in five out of six uterine cancer cell lines, as judged from Hoechst nuclear staining and effector caspase cleavage.
Our results showed the opposite, and this suggests that low-dose induction of proliferation by resveratrol is not mediated through the ER pathway.
Quercetin also induced the cleavage of caspase-3, caspase-7 and PARP (poly ADP-ribose polymerase).
Quercetin-induced phosphorylation of c-Jun N-terminal kinase (JNK) and cleavage of caspase-3 occurred 6 h after quercetin exposure and before cleavage of caspase-7 and PARP was detected.
Inhibition of MEK1/2 but not PI-3 kinase, p38 kinase or JNK abolished quercetin-induced phosphorylation of c-Jun, cleavage of caspase-3 and -7, cleavage of PARP and apoptosis.
The results suggest that in addition to inactivation of Akt-1 and alteration in the expression of the Bcl-2 family of proteins, activation of MEK-ERK is required for quercetin-induced apoptosis in A549 lung carcinoma cells.
Effect of cell signaling inhibitors on cell elongation induced by resveratrol
The resveratrol-induced cellular changes could represent a mechanism of minimizing endothelial damage by shearing forces in vivo.
Further insights into the nature of the resveratrol-induced morphologcial changes came from studies using selective inhibitors for different signaling pathways.
We observed that resveratrolinduced significant cellular and biochemical changes in endothelial cells, which were accompanied by altered functional responsiveness to conditions simulating arterial flow.
Bcl-XL overexpression prevented resveratrol-induced disruption of mitochondrial transmembrane potential (DeltaPsi(m)) and apoptosis.
Cells deficient in Fas/CD95 did not undergo resveratrol-induced apoptosis.
Pretreatment of MM cells with interferon-gamma upregulated Fas/CD95 and caspase-8, and potentiated resveratrol-induced apoptosis.
A FADD dominant-negative mutant, that blocked Fas/CD95 downstream signaling, precluded resveratrol-induced DeltaPsi(m) loss and apoptosis, indicating a sequence of Fas/CD95 signaling-->mitochondrion in the apoptotic response triggered by resveratrol.
We therefore asked what role, if any, Bax might have in the resveratrol-induced apoptosis of HCT116 cells.
Our results show that the lack of Bax in HCT116 colon carcinoma cells attenuates but fails to completely inhibit the resveratrol-induced mitochondrial form of apoptosis.
The expression, subcellular localization, and importance of Bax for resveratrol-provoked apoptosis were assessed in human HCT116 colon carcinoma cells and derivatives with both bax alleles inactivated.
Active Bax located at the mitochondria can mediate apoptosis , and we have recently reported that resveratrol can indeed trigger the mitochondrion form of death in HCT116 cells .
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