<i><scp>SIRT</scp>2</i> knockdown increases basal autophagy and prevents postslippage death by abnormally prolonging the mitotic arrest that is induced by microtubule inhibitors

Inoue, Toshiaki; Nakayama, Yuji; Li, Yanze; Matsumori, Haruka; Takahashi, Haruka; Kojima, Hiroyuki; Wanibuchi, Hideki; Katoh, Motonobu; Oshimura, Mitsuo

doi:10.1111/febs.12810

Cited by 55 publications

(36 citation statements)

References 51 publications

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“…Sirt1 and Sirt2 have also been implicated in autophagy. 25,26 Knockdown of Sirt1, but not Sirt2, decreased the TβRI level ( Figure VIIC and VIID in the online-only Data Supplement).…”

Section: Sirt7 Maintains Tβri Protein By Interacting With Protein Intmentioning

confidence: 94%

Sirt7 Contributes to Myocardial Tissue Repair by Maintaining Transforming Growth Factor-β Signaling Pathway

et al. 2015

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Background— Sirt7, 1 of the 7 members of the mammalian sirtuin family, promotes oncogenic transformation. Tumor growth and metastasis require fibrotic and angiogenic responses. Here, we investigated the role of Sirt7 in cardiovascular tissue repair process. Methods and Results— In wild-type mice, Sirt7 expression increased in response to acute cardiovascular injury, including myocardial infarction and hind-limb ischemia, particularly at the active wound healing site. Compared with wild-type mice, homozygous Sirt7-deficient (Sirt7 −/− ) mice showed susceptibility to cardiac rupture after myocardial infarction, delayed blood flow recovery after hind-limb ischemia, and impaired wound healing after skin injury. Histological analysis showed reduced fibrosis, fibroblast differentiation, and inflammatory cell infiltration in the border zone of infarction in Sirt7 −/− mice. In vitro, Sirt7 −/− mouse–derived or Sirt7 siRNA–treated cardiac fibroblasts showed reduced transforming growth factor-β signal activation and low expression levels of fibrosis-related genes compared with wild-type mice–derived or control siRNA–treated cells. These changes were accompanied by reduction in transforming growth factor receptor I protein. Loss of Sirt7 activated autophagy in cardiac fibroblasts. Transforming growth factor-β receptor I downregulation induced by loss of Sirt7 was blocked by autophagy inhibitor, and interaction of Sirt7 with protein interacting with protein kinase-Cα was involved in this process. Conclusion— Sirt7 maintains transforming growth factor receptor I by modulating autophagy and is involved in the tissue repair process.

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“…Sirt1 and Sirt2 have also been implicated in autophagy. 25,26 Knockdown of Sirt1, but not Sirt2, decreased the TβRI level ( Figure VIIC and VIID in the online-only Data Supplement).…”

Section: Sirt7 Maintains Tβri Protein By Interacting With Protein Intmentioning

confidence: 94%

Sirt7 Contributes to Myocardial Tissue Repair by Maintaining Transforming Growth Factor-β Signaling Pathway

et al. 2015

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“…Mitotic catastrophe is a complex oncosuppressive mechanism that is thought to sense mitotic failure and respond by driving cells toward an irreversible fate, be it apoptosis, necrosis, or senescence (148). Autophagy has been shown to facilitate cell survival during mitotic catastrophe (149, 150). Interestingly, during DNA damage-activated mitotic arrest, the previously identified mitosis-related CDK1-mediated phosphorylation of Vps34 on Thr159 (118) promotes Vps34 ubiquitination and proteasomal degradation (80).…”

Section: Cell Division and Autophagymentioning

confidence: 99%

Autophagy and the Cell Cycle: A Complex Landscape

2017

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Autophagy is a self-degradation pathway, in which cytoplasmic material is sequestered in double-membrane vesicles and delivered to the lysosome for degradation. Under basal conditions, autophagy plays a homeostatic function. However, in response to various stresses, the pathway can be further induced to mediate cytoprotection. Defective autophagy has been linked to a number of human pathologies, including neoplastic transformation, even though autophagy can also sustain the growth of tumor cells in certain contexts. In recent years, a considerable correlation has emerged between autophagy induction and stress-related cell-cycle responses, as well as unexpected roles for autophagy factors and selective autophagic degradation in the process of cell division. These advances have obvious implications for our understanding of the intricate relationship between autophagy and cancer. In this review, we will discuss our current knowledge of the reciprocal regulation connecting the autophagy pathway and cell-cycle progression. Furthermore, key findings involving nonautophagic functions for autophagy-related factors in cell-cycle regulation will be addressed.

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“…Data were acquired using BD LSRFortessa X-20 flowcytometer (BD Biosciences) equipped with 405 nm violet laser, and analyzed using FlowJo software (Tomy Digital Biology, Tokyo, Japan). Simultaneous evaluation of DNA content and phosphorylated mitotic protein was also analyzed by flowcytometry using anti-MPM2 antibody (Merck Millipore, Darmstadt, Germany) as previously reported (Inoue et al, 2014). Data were acquired using Gallios flowcytometer (Beckman Coulter, Brea, CA, USA) equipped with 488 nm blue and 633 nm red lasers.…”

Section: Flowcytometrymentioning

confidence: 99%

Recurrent Micronucleation through Cell Cycle Progression in the Presence of Microtubule Inhibitors

Nakayama

Uno

et al. 2015

Cell Struct. Funct.

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ABSTRACT. Although most cell lines undergo mitotic arrest after prolonged exposure to microtubule inhibitors, some cells subsequently exit this state and become tetraploid. Among these cells, limited numbers of rodent cells are known to undergo multinucleation to generate multiple small independent nuclei, or micronuclei by prolonged colcemid treatment. Micronuclei are thought to be formed when cells shift to a pseudo G1 phase, during which the onset of chromosomal decondensation allows individual chromosomes distributed throughout the cell to serve as sites for the reassembly of nuclear membranes. To better define this process, we used longterm live cell imaging to observe micronucleation induced in mouse A9 cells by treating with the microtubule inhibitor colcemid. Our observations confirm that nuclear envelope formation occurs when mitotic-arrested cells shift to a pseudo G1 phase and adopt a tetraploid state, accompanied by chromosome decondensation. Unexpectedly, only a small number of cells containing large micronuclei were formed. We found that tetraploid micronucleated cells proceeded through an additional cell cycle, shifting to a pseudo G1 phase and forming octoploid micronucleated cells that were smaller and more numerous compared with the tetraploid micronucleated cells. Our data suggest that micronucleation occur when cells shift from mitotic arrest to a pseudo G1 phase, and demonstrate that, rather than being a single event, micronucleation is an inducible recurrent process that leads to the formation of progressively smaller and more numerous micronuclei.

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SIRT2 knockdown increases basal autophagy and prevents postslippage death by abnormally prolonging the mitotic arrest that is induced by microtubule inhibitors

Cited by 55 publications

References 51 publications

Sirt7 Contributes to Myocardial Tissue Repair by Maintaining Transforming Growth Factor-β Signaling Pathway

Sirt7 Contributes to Myocardial Tissue Repair by Maintaining Transforming Growth Factor-β Signaling Pathway

Autophagy and the Cell Cycle: A Complex Landscape

Recurrent Micronucleation through Cell Cycle Progression in the Presence of Microtubule Inhibitors

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