2012
DOI: 10.1016/j.mad.2012.07.002
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Two mechanisms underlying the loss of p16Ink4a function are associated with distinct tumorigenic consequences for WS MEFs escaping from senescence

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Cited by 13 publications
(15 citation statements)
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“…Thus, RC-6 induced some cells to give rise to cellular senescence. Previous studies indicated that p16, p21 and p27 are related to cellular senescence in senescence cells (49)(50)(51)(52)(53). Therefore, these proteins were determined in the present study.…”
Section: Senescence Characteristics In Nt2 Cells After Rc-6 Treatmentmentioning
confidence: 88%
See 1 more Smart Citation
“…Thus, RC-6 induced some cells to give rise to cellular senescence. Previous studies indicated that p16, p21 and p27 are related to cellular senescence in senescence cells (49)(50)(51)(52)(53). Therefore, these proteins were determined in the present study.…”
Section: Senescence Characteristics In Nt2 Cells After Rc-6 Treatmentmentioning
confidence: 88%
“…Previous studies indicated that β-galactosidase activity is a major characteristic found in senescence cells and is generally applied to senescence detection (65)(66)(67). In addition, many studies have reported that p16 and p21 protein levels are increased in senescence cells (50)(51)(52)(53). At present, a small fraction of RC-6-treated NT2 cells can express β-galactosidase activity.…”
Section: Discussionmentioning
confidence: 99%
“…In summary, our current study demonstrates the clinicopathological significance of the p16-cyclin D1-Rb pathway and the MIB-1 level in skull base chordoma and chondrosarcoma. We believe that therapies targeting the cell cycle regulation, by exogenous over-expression of p16, 20 , 24 or introduction of the anti-sense oligonucleotides of cyclin D1, 25 or interference of Rb activity, may prove valuable in the treatment of cancer. 26 In addition, the molecular mechanisms involved in the Rb pathway (CDK4/6 pathway) and tumorigenesis of skull base tumors are being researched.…”
Section: Discussionmentioning
confidence: 99%
“…Senescent cells are prone to escape senescence by disrupting the function of the DDR pathway, mainly by mutating the p53 gene or other checkpoint regulatory genes. For example, when mouse WS embryonic fibroblast cells senesce, the cells are prone to escape senescence and re‐enter the cell cycle by either mutating p53 or deleting the genomic fragment of the Ink4A locus [Jia et al, ; Wu et al, ]. These studies have revealed a key role of the p53 gene status and DDR pathway in the surveillance of abnormal proliferation and utilizing cellular senescence against tumorigenesis.…”
Section: Crosstalk In the Molecular Pathway Regulating Aging And Tumomentioning
confidence: 99%
“…The time point and the status of cells for interference might be the key for determining the consequent longevity or tumor growth. Another possible strategy for reducing the stress of the cellular surveillance system was reducing the expression level of p16Ink4a while not affecting p53 [Wu et al, ].…”
Section: Crosstalk In the Molecular Pathway Regulating Aging And Tumomentioning
confidence: 99%