We are analyzing https://link.springer.com/article/10.1007/s10495-005-2948-y.

Title:
Caspase-independent apoptosis is activated by diazepam-induced mitotic failure in HeLa cells, but not in human primary fibroblasts | Apoptosis
Description:
DZ, a benzodiazepine known to affect centrosome separation at prophase, leads to a higher degree of mitotic arrest in HeLa cells than in primary human fibroblasts. In fact, differently from fibroblasts, which undergo a transient block in prophase-to-prometaphase transition, a high proportion of tumor cells attempt to escape from the DZ-imposed mitotic block, fail to undergo complete mitosis and die by mitotic failure. DZ-treated samples showed certain biochemical hallmarks of apoptosis, such as induction of the proapototic Bax protein, mitochondrial alterations assessed by JC-1 staining and TEM analysis, PARP cleavage, and DNA fragmentation. However, in DZ-treated cells, we observed a very low or absent caspase activation as shown by immunofluorescence and immunoblot experiments with antibodies directed to activated caspases and by staining with the pancaspase inhibitor FITC-VAD-FMK. Experiments on mitochondrial depolymerization and apoptosis induction carried out in the presence of specific inhibitors of caspase-2 and caspase-3/7 indicated a caspase-independent apoptotic process induced by DZ. Accordingly, TEM analysis of treated cells revealed ultrastructural features resembling those reported for caspase-independent apoptosis. In conclusion, we hypothesize that HeLa cells override the prophase block imposed by DZ, producing a high rate of aberrant pro-metaphases, which, in turn, activates caspase-independent, apoptosis-like mitotic catastrophe.
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Keywords {🔍}

google, scholar, pubmed, article, cell, apoptosis, mitotic, cells, cancer, death, res, caspaseindependent, human, mitochondrial, caspase, oncogene, catastrophe, nature, hela, antoccia, agents, biol, privacy, cookies, content, analysis, induction, spindle, chromosome, checkpoint, diazepam, function, publish, search, fibroblasts, tanzarella, benzodiazepine, centrosome, arrest, access, induces, kinase, role, lung, clin, data, information, log, journal, research,

Topics {✒️}

pancaspase inhibitor fitc-vad-fmk caspase-independent cell death radiation-induced cell death month download article/chapter diazepam-induced mitotic failure cell-cycle arrest dz-treated samples showed mitochondrial apoptosis-inducing factor apoptotic cell death dz-imposed mitotic block small molecule inhibitor human lung cancers related subjects potential anticancer agents full article pdf caspase-independent apoptosis activates caspase-independent caspase-independent routes article apoptosis aims peripheral benzodiazepine receptors suspected spindle poisons privacy choices/manage cookies mitotic catastrophe constitutes microtubule-interfering agents anti-microtubule agents g2 checkpoint control undergo complete mitosis h2o2-induced apoptosis dz-treated cells affect centrosome separation proapototic bax protein microtubule stabilizing agents apoptotic pathways plays primary human fibroblasts human primary fibroblasts caspase-inhibited neurons hela s3 cells cell death tumor cells attempt chinese hamster cells mitochondrial membrane potential evaluating centrosome function hela cells override absent caspase activation mitochondrial alterations assessed mitochondrial channel vdac dna damage checkpoint european economic area scope submit manuscript aberrant pro-metaphases

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Caspase-independent cell death?

Schema {🗺️}

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         headline:Caspase-independent apoptosis is activated by diazepam-induced mitotic failure in HeLa cells, but not in human primary fibroblasts
         description:DZ, a benzodiazepine known to affect centrosome separation at prophase, leads to a higher degree of mitotic arrest in HeLa cells than in primary human fibroblasts. In fact, differently from fibroblasts, which undergo a transient block in prophase-to-prometaphase transition, a high proportion of tumor cells attempt to escape from the DZ-imposed mitotic block, fail to undergo complete mitosis and die by mitotic failure. DZ-treated samples showed certain biochemical hallmarks of apoptosis, such as induction of the proapototic Bax protein, mitochondrial alterations assessed by JC-1 staining and TEM analysis, PARP cleavage, and DNA fragmentation. However, in DZ-treated cells, we observed a very low or absent caspase activation as shown by immunofluorescence and immunoblot experiments with antibodies directed to activated caspases and by staining with the pancaspase inhibitor FITC-VAD-FMK. Experiments on mitochondrial depolymerization and apoptosis induction carried out in the presence of specific inhibitors of caspase-2 and caspase-3/7 indicated a caspase-independent apoptotic process induced by DZ. Accordingly, TEM analysis of treated cells revealed ultrastructural features resembling those reported for caspase-independent apoptosis. In conclusion, we hypothesize that HeLa cells override the prophase block imposed by DZ, producing a high rate of aberrant pro-metaphases, which, in turn, activates caspase-independent, apoptosis-like mitotic catastrophe.
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      headline:Caspase-independent apoptosis is activated by diazepam-induced mitotic failure in HeLa cells, but not in human primary fibroblasts
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      dateModified:
      pageStart:909
      pageEnd:920
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         caspase-3
         caspase-9
         cell death
         centrosome
         diazepam
         mitotic catastrophe
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
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