Effects of diverse dietary phytoestrogens on cell growth, cell cycle and apoptosis in estrogen-receptor-positive breast cancer cells

Sakamoto, Takako; Horiguchi, Hyogo; Oguma, Etsuko; Kayama, Fujio

doi:10.1016/j.jnutbio.2009.06.010

Cited by 135 publications

(101 citation statements)

References 47 publications

(73 reference statements)

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“…In the MCF-7 breast cancer cell line treated with 10-5 M resveratrol, the reduction of the Bcl-2/Bax ratio through enhancement of p53-dependent transcriptional activity at least partially contributes to resveratrol's pro-apoptotic activity in this research (19). A similar effect and mechanism could also be found in MCF-7 and MDA-MB231 breast cancer cells treated with resveratrol where the up-regulation of Bax and p21 resulted from the up-regulation of ASPP1 (apoptosis stimulation protein of p53 1) (20).…”

Section: Intrinsic Pathway Of Apoptosismentioning

confidence: 67%

“…As for the role of p53 as a transcription factor, resveratrol could reduce the Bcl-2/Bax ratio through regulating the Bcl-2 and Bax promoters by affecting transcription factors p53 and NF-κB differently: enhancing p53-dependent transcriptional activity and reducing the NF-κB-dependent transcriptional activity (19). In A549 non-small cell lung cancer (NSCLC) cells treated with benzopyrene and/or resveratrol, resveratrol down-regulated IKK and NF-κB, causing decrease in the expression of cyclinD1, in which process the upregulation of p53 and p21 also contributed to it.…”

Section: Apoptosis Led By Cell Cycle Arrest: Importance Of P53 and P21mentioning

confidence: 99%

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Anti-tumor effects and cellular mechanisms of resveratrol

Han

Xia

Gao

et al. 2015

DD&T

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Section: Intrinsic Pathway Of Apoptosismentioning

confidence: 67%

Section: Apoptosis Led By Cell Cycle Arrest: Importance Of P53 and P21mentioning

confidence: 99%

Anti-tumor effects and cellular mechanisms of resveratrol

Han

Xia

Gao

et al. 2015

DD&T

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“…Several strategies such as distal aortic perfusion, intrathecal vasodilators, reattachment of intercostal and lumbar vessels, and decreasing cerebrospinal fluid pressure have been used to overcome the hypoperfusion. Other measures including the free radical scavengers and immune system modulation also help to decrease the reperfusion injury (1,10,19,21).…”

Section: Caspase-3 Expression Of Sciatic Nerve Fibersmentioning

confidence: 99%

The axon protective effects of syringic acid on ischemia/reperfusion injury in a rat sciatic nerve model

Tokmak¹,

Şehitoğlu²,

Yüksel³

et al. 2015

Turkish Neurosurgery

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“…Resveratrol is an established cytotoxic agent in prostate, 23 breast, 33 ovarian, 34 colon, 35 lung, 36 heptatic, and brain cancer cells 37 and is a proposed chemopreventive agent. 22 As a component of grape skins, resveratrol is already in the diet, 38 implying it may be well tolerated if used in long-term clinical dosing.…”

Section: U0126 Inhibits Resveratrol Induced Apoptosismentioning

confidence: 99%

A metabolic perturbation by U0126 identifies a role for glutamine in resveratrol-induced cell death

Freeman

Kim

Lisanti

et al. 2011

Cancer Biology & Therapy

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Recent evidence has identified substantial overlap between metabolic and oncogenic biochemical pathways, suggesting novel approaches to cancer intervention. For example, cholesterol lowering statins and the antidiabetes medication metformin both act as chemopreventive agents in prostate and other cancers. The natural compound resveratrol has similar properties: increasing insulin sensitivity, suppressing adipogenesis, and inducing apoptotic death of cancer cells in vitro. However, in vivo tumor xenografts acquire resistance to resveratrol by an unknown mechanism, while mouse models of metabolic disorders respond more consistently to the compound. Here we demonstrate that castrationresistant human prostate cancer C4-2 cells are more sensitive to resveratrol-induced apoptosis than isogenic androgendependent LNCaP cells. The MEK inhibitor U0126 antagonized resveratrol-induced apoptosis in C4-2 cells, but this effect was not seen with other MEK inhibitors. U0126 was found to inhibit mitochondrial function and shift cells to aerobic glycolysis independently of MEK. Mitochondrial activity of U0126 arose through decomposition, producing both mitochondrial fluorescence and cyanide, a known inhibitor of complex IV. Applying U0126 mitochondrial inhibition to C4-2 cell apoptosis, we tested the possibility that glutamine supplementation of citric acid cycle intermediate aketoglutarate may be involved. Suppression of the conversion of glutamate to a-ketoglutarate antagonized resveratrolinduced death in C4-2 cells. A similar effect was also seen by reducing extracellular glutamine concentration in the culture medium, suggesting that resveratrol-induced death is dependent on glutamine metabolism, a process frequently dysregulated in cancer. Further work on resveratrol and metabolism in cancer is warranted to ascertain if the glutamine dependence has clinical implications.

show abstract

Effects of diverse dietary phytoestrogens on cell growth, cell cycle and apoptosis in estrogen-receptor-positive breast cancer cells

Cited by 135 publications

References 47 publications

Anti-tumor effects and cellular mechanisms of resveratrol

Anti-tumor effects and cellular mechanisms of resveratrol

The axon protective effects of syringic acid on ischemia/reperfusion injury in a rat sciatic nerve model

A metabolic perturbation by U0126 identifies a role for glutamine in resveratrol-induced cell death

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