We are analyzing https://link.springer.com/article/10.1007/s10495-008-0200-2.

Title:
The tubulin-depolymerising agent combretastatin-4 induces ectopic aster assembly and mitotic catastrophe in lung cancer cells H460 | Apoptosis
Description:
The relationship between microtubular dynamics, dismantling of pericentriolar components and induction of apoptosis was analysed after exposure of H460 non-small lung cancer cells to anti-mitotic drugs. The microtubule destabilising agent, combretastatin-A4 (CA-4) led to microtubular array disorganization, arrest in mitosis and abnormal metaphases, accompanied by the presence of numerous centrosome-independent “star-like” structures containing tubulin and aggregates of pericentrosomal matrix components like γ-tubulin, pericentrin and ninein, whereas the structural integrity of centrioles was not affected by treatment. On the contrary, in condition of prolonged exposure or high concentrations of CA-4 such aggregates never formed. Treatment with 7.5 nM CA-4, which produced a high frequency “star-like” aggregates, was accompanied by mitotic catastrophe commitment characterized by translocation of the proapoptotic Bim protein to mitochondria activation of caspases-3/9 and DNA fragmentation as a result of either prolonged metaphase arrest or attempt of cells to divide. Drug concentrations which fail to block cells at mitosis were also unable to activate apotosis. A detailed time-course analysis of cell cycle arrest and apoptosis indicated that after CA-4 washout the number of metaphases with “star-like” structures decreased as a function of time and arrested cells proceeded in anaphase. After 4 h, the multiple α- and γ-tubulin aggregates coalesced into two well-defined spindles in a bipolar mitotic spindle organization. Overall, our findings suggest that the maintenance of microtubular integrity plays a relevant role in stabilising the pericentriolar matrix, whose dismantling can be associated with apoptosis after exposure to microtubule depolymerising agents.
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Keywords {🔍}

google, scholar, cas, pubmed, article, cell, cells, mitotic, biol, microtubule, centrosome, apoptosis, catastrophe, sci, gammatubulin, spindle, role, microtubules, cancer, centrosomal, privacy, cookies, combretastatin, induces, cenciarelli, tanzarella, vitale, antoccia, arrest, mitosis, ninein, agents, death, rev, centrosomes, bornens, function, content, publish, search, agent, lung, crateri, arancia, dynamics, tubulin, aggregates, γtubulin, pericentrin, protein,

Topics {✒️}

month download article/chapter radiation-induced cell death radiation-induced mitotic catastrophe diazepam-induced mitotic failure microtubule-organizing centers abnormal microtubule minus-end anchorage gamma-tubulin complexes x-irradiated mammalian cells stefania meschini & giuseppe arancia arsenite-induced mitotic arrest microtubule destabilising agent numerous centrosome-independent “star proapoptotic bim protein microtubule depolymerising agents γ-tubulin aggregates coalesced p53 transcription-dependent full article pdf gamma-tubulin form microtubulin binding sites article apoptosis aims privacy choices/manage cookies gamma-tubulin distribution cell cycle arrest kinetochore-microtubule attachment tubulin superfamily encoded alpha tubulin acetylation ilio vitale article cenciarelli minus-end capture antonio antoccia combretastatin-a4 multinucleated cells induced incresased microtubule stability independent processes linked sigma-tau anti-mitotic drugs microtubule-interfering agents microtubule-damaging agents microtubular array disorganization arrested cells proceeded european economic area microtubular integrity plays vande woude gf adenomatous polyposis coli combretastatin ca-4 crest patient sera mitochondrial membrane permeabilization università roma tre university “roma tre” microtubule anchoring mechanisms

Questions {❓}

Roninson IB, Broude EV, Chang BD (2007) If not apoptosis then what?

Schema {🗺️}

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         description:The relationship between microtubular dynamics, dismantling of pericentriolar components and induction of apoptosis was analysed after exposure of H460 non-small lung cancer cells to anti-mitotic drugs. The microtubule destabilising agent, combretastatin-A4 (CA-4) led to microtubular array disorganization, arrest in mitosis and abnormal metaphases, accompanied by the presence of numerous centrosome-independent “star-like” structures containing tubulin and aggregates of pericentrosomal matrix components like γ-tubulin, pericentrin and ninein, whereas the structural integrity of centrioles was not affected by treatment. On the contrary, in condition of prolonged exposure or high concentrations of CA-4 such aggregates never formed. Treatment with 7.5 nM CA-4, which produced a high frequency “star-like” aggregates, was accompanied by mitotic catastrophe commitment characterized by translocation of the proapoptotic Bim protein to mitochondria activation of caspases-3/9 and DNA fragmentation as a result of either prolonged metaphase arrest or attempt of cells to divide. Drug concentrations which fail to block cells at mitosis were also unable to activate apotosis. A detailed time-course analysis of cell cycle arrest and apoptosis indicated that after CA-4 washout the number of metaphases with “star-like” structures decreased as a function of time and arrested cells proceeded in anaphase. After 4 h, the multiple α- and γ-tubulin aggregates coalesced into two well-defined spindles in a bipolar mitotic spindle organization. Overall, our findings suggest that the maintenance of microtubular integrity plays a relevant role in stabilising the pericentriolar matrix, whose dismantling can be associated with apoptosis after exposure to microtubule depolymerising agents.
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