Prolonged unbalanced growth induces cellular senescence markers linked with mechano transduction in normal and tumor cells

Sumikawa, Emi; Matsumoto, Yuko; Sakemura, Risa; Fujii, Michihiko; Ayusawa, Dai

doi:10.1016/j.bbrc.2005.07.106

Cited by 34 publications

(39 citation statements)

References 34 publications

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“…A similar inverse relationship between the cell size and number of cell divisions has been noted previously for human fibroblasts in culture (Angello et al 1987(Angello et al , 1989 and, more recently, for normal and neoplastic cells under conditions of prolonged unbalanced growth induced by suppression of cell divisions (Sumikawa et al 2005).…”

Section: Resultsmentioning

confidence: 66%

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

et al. 2008

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The number of cell divisions of the yeast Saccharomyces cerevisiae is limited, referred to as "replicative lifespan" of this organism and believed to be due to aging mechanisms similar to those of mammalian cells. We demonstrate, using three pairs of isogenic yeast strains (standard and a mutant deficient in an antioxidant defense protein) that although the lifespan differs significantly, the final volume attained after the last division is similar within each pair of strains. In a population, cells cease to bud after various number of cell cycles but attaining a similar final volume. These results indicate that the increase in the mother cell volume, intrinsic to the asymmetric cell division in S. cerevisiae, may be the main mechanism limiting the reproductive capacity of in this organism.

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Section: Resultsmentioning

confidence: 66%

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

et al. 2008

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“…Cellular senescence can also be induced by various means such as oxidative stress, DNA damages, cell-cycle perturbation, chromatin destabilization, and signaling imbalances (Herbig and Sedivy 2006;Sumikawa et al 2005;Kobayashi et al 2008). Therefore, epigenetic factors together with genetic factors may play an important role during senescence in normal individuals.…”

Section: Introductionmentioning

confidence: 98%

Coordinate expression of the human pregnancy-specific glycoprotein gene family during induced and replicative senescence

et al. 2008

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Pregnancy-specific glycoproteins (PSGs) comprise a family of highly similar polypeptides encoded by 11 transcriptionally active genes that compactly cluster on band 19q13.2. All members of the PSG family were found to be markedly up-regulated by addition of 5-bromodeoxyuridine in HeLa cells. Similarly, all of the members were markedly up-regulated during replicative senescence in normal human fibroblasts. Promoter analysis of the PSG1, 4, and 11 genes in HeLa cells did not reveal a cis-regulatory element responsive to 5-bromodeoxyuridine in their 5'-flanking sequences. These results suggest that the PSG genes are regulated at a level of higher order chromatin structure besides by a signal of pregnancy.

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“…In normal human fibroblasts entering replicative senescence, p38 and JNK stress-activated kinases are also activated in addition of ERK1/2, suggesting a number of external stresses are imposed on senescent cells (Sumikawa et al 2005). Our earlier study clearly shows that cardiolipin inhibits cell growth and strongly induces senescence-associated b-galasctosidase and senescence marker genes such as those encoding p21 waf1/SdiÀ1 , fibronectin, and collagenase after culture for 1-2 weeks in the presence of appropriate concentrations of cardiolipin (Arivazhagan .…”

Section: Resultsmentioning

confidence: 99%

Cardiolipin activates MAP kinases during premature senescence in normal human fibroblasts

Arivazhagan

Ayusawa

2007

Biogerontology

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Lipids are major structural components of cellular membranes and regulate various signaling pathways as a mediator of the signals or a source of new signals. Our earlier studies show that cardiolipin very sensitively induces premature senescence in normal human fibroblasts. To understand a molecular basis for the action of cardiolipin, we tested whether the mitogen-activated protein (MAP) kinase cascades have a role in the above phenomenon. As expected, cardiolipin activated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK), and p38 map kinase (p38) of the MAP kinase family as in replicatively senesced cells. These results suggest that cardiolipin uses signaling pathways similar to those in replicative senescence to lead to premature senescence.

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Prolonged unbalanced growth induces cellular senescence markers linked with mechano transduction in normal and tumor cells

Cited by 34 publications

References 34 publications

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

Coordinate expression of the human pregnancy-specific glycoprotein gene family during induced and replicative senescence

Cardiolipin activates MAP kinases during premature senescence in normal human fibroblasts

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