23 research outputs found
Microtubule Organization Requires Cell Cycle-dependent Nucleation at Dispersed Cytoplasmic Sites: Polar and Perinuclear Microtubule Organizing Centers in the Plant Pathogen Ustilago maydis
Centrosome Behavior under the Action of a Mitochondrial Uncoupler and the Effect of Disruption of Cytoskeleton Elements on the Uncoupler-Induced Alterations
Centrosome Behavior under the Action of a Mitochondrial Uncoupler and the Effect of Disruption of Cytoskeleton Elements on the Uncoupler-Induced Alterations
Cancer cells response on the microtubuler-inhibiting drugs
Cancer is one of the age-related diseases with detrimental impact on people
survival. Improvement of cancer therapies is a major focus of many scientists around the world.
Anticancer drugs based on the microtubules inhibition are successfully used to treat widerange
of cancers. Anti-microtubules drugs directly bind to colchicine, vinca and taxol binding
sites on beta-tubulin, resulting in the impairment of spindle formation, vesicle transport, cell
structure and migration. One of the modes of action anti-tubulin drugs is through causing faults
in mitotic spindle function, which lead to the prolonged mitotic block and consequently to cell
death. Although, drugs' high toxicity and development of resistance in patients lead to the idea
of revisiting the dosage and combination therapies of anti-tubulin drugs, some sources reported
that cell migration is more sensitive to microtubule inhibiting drugs than to cell proliferation
in endothelial cells. Previously, we reported observations on NIH/3T3 (normal fibroblasts) cell
proliferative activity, cell migration and direct test of microtubule dynamics. Thus, we aimed to
identify effect of microtubule inhibitors on cancer cell lines. In addition, we compare normal cell
lines with human cancer cell lines such as A549 (lung carcinoma), HT1080 (fibrosarcoma) and
U118 (glioma)
Optical trapping for chromosome manipulation: a wavelength dependence of induced chromosome bridges
Using a tunable titanium-sapphire laser, we have compared different wavelengths (from 700 to 840 nm) for their utility in optical trapping of chromosomes in mitotic rat kangaroo Potorous tridactylus (PtK2) cells. It was found that irradiation with a near-infrared light induces the sticking together of chromosome shoulders. The attached chromatids failed to separate, or separated with significant delay and formed a chromosome bridge during anaphase. Using this bridge (and induced c-mitosis) as a reference, we compared the action of different wavelengths (from 700 to 840 nm). Chromosomes were irradiated at metaphase and the cells were observed until the end of cytokinesis. Chromosomes were irradiated for different periods of time, using 130 mW of power at the objective focal plane. The biological responses observed after optical trapping were: (1) normal cell division, (2) formation of a temporary chromosome bridge, (3) formation of a permanent chromosome bridge, (4) complete blockage of chromosome separation (c-mitosis). The chromosomes were found to have a maximal sensitivity to 760–765 nm light and minimal sensitivity to 700 and 800–820 nm light. Cells with chromosomes irradiated for a long time, using wavelength 760–765 nm, generally were incapable of going through anaphase and remained in c-mitosis. We conclude that the optimal wavelengths for optical trapping are 700 and 800–820 nm
Cancer cells response on the microtubuler-inhibiting drugs
Cancer is one of the age-related diseases with detrimental impact on people
survival. Improvement of cancer therapies is a major focus of many scientists around the world.
Anticancer drugs based on the microtubules inhibition are successfully used to treat widerange
of cancers. Anti-microtubules drugs directly bind to colchicine, vinca and taxol binding
sites on beta-tubulin, resulting in the impairment of spindle formation, vesicle transport, cell
structure and migration. One of the modes of action anti-tubulin drugs is through causing faults
in mitotic spindle function, which lead to the prolonged mitotic block and consequently to cell
death. Although, drugs' high toxicity and development of resistance in patients lead to the idea
of revisiting the dosage and combination therapies of anti-tubulin drugs, some sources reported
that cell migration is more sensitive to microtubule inhibiting drugs than to cell proliferation
in endothelial cells. Previously, we reported observations on NIH/3T3 (normal fibroblasts) cell
proliferative activity, cell migration and direct test of microtubule dynamics. Thus, we aimed to
identify effect of microtubule inhibitors on cancer cell lines. In addition, we compare normal cell
lines with human cancer cell lines such as A549 (lung carcinoma), HT1080 (fibrosarcoma) and
U118 (glioma)
