ArticleCurrent biology : CB2007
The G2 p38-mediated stress-activated checkpoint pathway becomes attenuated in transformed cells.
Article in Current biology : CB, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 19 citations in OpenAlex.
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- Review
- The Chinese herb isolate yuanhuacine (YHL-14) induces G2/M arrest in human cancer cells by up-regulating p21 protein expression through an p53 protein-independent cascade.The Journal of biological chemistry · 2014Article
- Chemo-sensitisation of HeLa cells to etoposide by a benzoxazine in the absence of DNA-PK inhibition.Investigational new drugs · 2013Article
- A prognostic signature of G(2) checkpoint function in melanoma cell lines.Cell cycle (Georgetown, Tex.) · 2013Article
- Low-dose anisomycin sensitizes melanoma cells to TRAIL induced apoptosis.Cancer biology & therapy · 2013Article
- Circumventing photodamage in live-cell microscopy.Methods in cell biology · 2013Review
- MK2 Regulates Ras Oncogenesis through Stimulating ROS Production.Genes & cancer · 2012Article
- p38α Signaling Induces Anoikis and Lumen Formation During Mammary Morphogenesis.Science signaling · 2011Article
- Mitosis in vertebrates: the G2/M and M/A transitions and their associated checkpoints.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2011Review
- Chromosomes and cancer cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2011Review
- Signaling through the P38 and ERK pathways: a common link between HIV replication and the immune response.Immunologic research · 2010Review
- p38 mitogen-activated protein kinase promotes cell survival in response to DNA damage but is not required for the G(2) DNA damage checkpoint in human cancer cells.Molecular and cellular biology · 2010Article
- Proliferation of aneuploid human cells is limited by a p53-dependent mechanism.The Journal of cell biology · 2010Article
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4 authors at 2 institutions in 1 country.
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Abstract
When human cells are stressed during G2, they are delayed from entering mitosis via a checkpoint mediated by the p38 kinase, and this delay can be modeled by the selective activation of p38 with anisomycin. Here, we report, on the basis of live-cell studies, that 75 nM anisomycin transiently (1 hr) activates p38 which, in turn, rapidly and completely blocks entry into mitosis for at least 4 hr in all primary, telomerase- or spontaneously immortalized (p53+ and pRB+) human cells. However, the same treatment does not delay entry into mitosis in cancer cells, or the delay in entering mitosis is shortened, even though it induces a similar transient and comparable (or stronger) activation of p38. Because the primary substrate of p38, the MK2 kinase, is also transiently (1-2 hr) activated by anisomycin in both normal and cancer cells, checkpoint disruption in transformed cells occurs downstream of MK2. Finally, observations on isogenic lines reveal that the duration of the stress checkpoint is shortened in cells lacking both p53 and pRb and that the constitutive expression of an active H-Ras oncogene in these cells further attenuates the checkpoint via an ERK1/2-dependent manner. Thus, transformation leads to attenuation of the p38-mediated stress checkpoint. This outcome is likely selected for during transformation because it confers the ability to outgrow normal cells under stressful in vitro (culture) or in vivo (tumor) environments. Our data caution against using cancer cells to study how p38 produces a G2 arrest.
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