Activation of SIRT1 by Resveratrol requires lamin A

Liu, Baohua; Zhou, Zhongjun

doi:10.18632/aging.100532

Cited by 12 publications

(8 citation statements)

References 8 publications

(8 reference statements)

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“…Resveratrol (trans 3, 4′, 5-trihydroxystilbene; RSV), a polyphenol phytoalexin found in grapes, peanuts and other plants, is well-known for its potential antioxidant, anti-tumorigenic activities [1–4], extends lifespan by activate Sirt1 [5, 6]. Accumulated reports demonstrate that RSV has the ability to affect tumor initiation and promotion, arrest angiogenesis and metastasis, and induce cell cycle arrest and apoptosis [7].…”

Section: Introductionmentioning

confidence: 99%

P62 Regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis

Zhang

et al. 2014

OncotargetHas erratum 2021-11-9 Has correction 2021-11-9

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Resveratrol is a potential polyphenol drug used in cancer treatment. We examined the relationship between autophagy and apoptosis in RSV-treated non-small lung adenocarcinoma A549 cells. Resveratrol treatment increased autophagy and autophagy-mediated degradation of P62. Immunocytochemistry revealed P62 co-localized with Fas/Cav-1 complexes, known to induce apoptosis. However, siRNA-mediated P62 downregulation enhanced formation of Fas/Cav-1 complexes, suggesting that P62 inhibited Fas/Cav-1 complex formation. Fas/Cav-1 complexes triggered caspase-8 activation and cleavage of Beclin-1, releasing a C-terminal Beclin-1 peptide that translocated to the mitochondria and initiate apoptosis. Inhibition of autophagy by siRNA-mediated repression of Beclin-1 also blocked RSV-induced apoptosis, showing a dependence of apoptosis on autophagy. P62 knockdown by siRNA accelerated the activation of caspase-8 and initiate apoptosis, while Cav-1 knockdown inhibited apoptosis, but increased autophagy. Inhibition of autophagy by 3-MA prevented both P62 degradation and induction of apoptosis, whereas inhibition of apoptosis by z-IETD-FMK or z-DEVD-FMK enhanced both P62 induction and autophagic cell death. In conclusion, P62 links resveratrol-induced autophagy to apoptosis. P62 blocks apoptosis by inhibiting Fas/Cav-1 complex formation, but RSV-induced autophagic degradation of P62 enables formation of Fas/Cav-1 complexes which then activate caspase-8-mediated Beclin-1 cleavage, resulting in translocation of the Beclin-1 C-terminal fragment to the mitochondria to initiate apoptosis.

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Section: Introductionmentioning

confidence: 99%

P62 Regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis

Zhang

et al. 2014

OncotargetHas erratum 2021-11-9 Has correction 2021-11-9

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“…Alterations in several histone‐modifying enzymes occur through the lifespan (reviewed in López‐Otín et al, 2013; Zane, Sharma, & Misteli, 2014), and among these are sirtuins (SIRTs), a family of NAD‐dependent deacetylases with multiple roles in metabolism, cancer, and aging (reviewed in López‐Otín et al, 2013). It is well accepted that both SIRT1 and SIRT6 are involved with longevity given their functions in genomic stability, metabolic regulation, and chromatin remodeling (Liu & Zhou, 2013) (Figure 2). Interestingly, SIRT1 activity is dependent of lamin A binding, but not on progerin or prelamin A binding.…”

Section: Chromatin Organizationmentioning

confidence: 99%

Nuclear envelope dysfunction and its contribution to the aging process

et al. 2020

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The nuclear envelope (NE) is the central organizing unit of the eukaryotic cell serving as a genome protective barrier and mechanotransduction interface between the cytoplasm and the nucleus. The NE is mainly composed of a nuclear lamina and a double membrane connected at specific points where the nuclear pore complexes (NPCs) form. Physiological aging might be generically defined as a functional decline across lifespan observed from the cellular to organismal level. Therefore, during aging and premature aging, several cellular alterations occur, including nuclear‐specific changes, particularly, altered nuclear transport, increased genomic instability induced by DNA damage, and telomere attrition. Here, we highlight and discuss proteins associated with nuclear transport dysfunction induced by aging, particularly nucleoporins, nuclear transport factors, and lamins. Moreover, changes in the structure of chromatin and consequent heterochromatin rearrangement upon aging are discussed. These alterations correlate with NE dysfunction, particularly lamins’ alterations. Finally, telomere attrition is addressed and correlated with altered levels of nuclear lamins and nuclear lamina‐associated proteins. Overall, the identification of molecular mechanisms underlying NE dysfunction, including upstream and downstream events, which have yet to be unraveled, will be determinant not only to our understanding of several pathologies, but as here discussed, in the aging process.

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“…Other beneficial effects attributed to resveratrol relate to aging, e.g., cataract and bone mass loss, and to neurodegeneration, obesity and diabetes [ 11 ]. Resveratrol induces expression of multiple genes and confers metabolic changes that mimic caloric restriction, a state which promotes longevity across species [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…These benefits appear to be dependent upon sirtuin 1 (SIRT1), a NAD + -dependent deacetylase. How resveratrol activates SIRT1 protein is not entirely clear, but the binding of lamin A by SIRT1 induces an allosteric change in SIRT1 that exposes its deacetylase site to native substrates [ 11 ]. Modulation of SIRT1 activity is also dependent on physiological substrate sequence and these substrates may contribute to actions of resveratrol [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Anti-proliferative and gene expression actions of resveratrol in breast cancer cells in vitro

et al. 2014

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We have used a perfusion bellows cell culture system to investigate resveratrolinduced anti-proliferation/apoptosis in a human estrogen receptor (ER)-negative breast cancer cell line (MDA-MB-231). Using an injection system to perfuse media with stilbene, we showed resveratrol (0.5 – 100 μM) to decrease cell proliferation in a concentration-dependent manner. Comparison of influx and medium efflux resveratrol concentrations revealed rapid disappearance of the stilbene, consistent with cell uptake and metabolism of the agent reported by others. Exposure of cells to 10 μM resveratrol for 4 h daily × 6 d inhibited cell proliferation by more than 60%. Variable extracellular acid-alkaline conditions (pH 6.8 – 8.6) affected basal cell proliferation rate, but did not alter anti-proliferation induced by resveratrol. Resveratrol-induced gene expression, including transcription of the most up-regulated genes and pro-apoptotic p53-dependent genes, was not affected by culture pH changes. The microarray findings in the context of induction of anti-proliferation with brief daily exposure of cells to resveratrol—and rapid disappearance of the compound in the perfusion system—are consistent with existence of an accessible initiation site for resveratrol actions on tumor cells, e.g., the cell surface receptor for resveratrol described on integrin αvβ3.

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Activation of SIRT1 by Resveratrol requires lamin A

Cited by 12 publications

References 8 publications

P62 Regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis

P62 Regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis

Nuclear envelope dysfunction and its contribution to the aging process

Anti-proliferative and gene expression actions of resveratrol in breast cancer cells in vitro

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