Microtubule Associated

Microscope image (406) magnification of U937 cells after exposure to SM-TNs. a) Untreated U937 cells. b) U937 cells treated with 200 nM, and 35 nM ODS empty shells. c) U937 cells treated with microcrystalline (free) Taxol prepared by sonicating Taxol in 20%H3PO4/0.8% SDS solution. d) U937 cells treated with 200 nM SM-TN. A SM-TN is seen in the middle of the picture. e) U937 cells treated with 35 nM SMTN.The nanowires are too small to see at this magnification, but their effect on the cells is clearly visible. Scale bar = 10 mm.

for HXO-RB44 cells, IC50 values for VCR were changed in the different SG600 treatment groups. The results are representative of three independent  experiments and of f our replicates in each experiment.

Matrigel invasion assay of H1299 cells treated with SDF-1α or SDF-1α plus Epothilone B prior to 0 or 2 Gy irradiation. After the treatment for 12 h, the H1299 cells that migrated to the bottom surface of the membrane were stained with Giemsa, and the number of migrated cells was calculated manually.

A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). Total cell lysates were probed with the indicated antibodies against Hippo components on Phos-tag SDS-polyacrylamide gels. O and * mark the non-phosphorylated and phosphorylated proteins, respectively.

ABCB1 functional inhibition using elacridar re-sensitizes TaxR and DU145-DTXR cells to cabazitaxel treatment. A. TaxR and DU145-DTXR cells were subjected to cell growth assays using either vehicle (DMSO), elacridar (0.5μM), cabazitaxel (1nM), or a combination of elacridar and cabazitaxel. Cells were counted 72 hours post-treatment. B. TaxR and DU145-DTXR cells were treated with either vehicle (DMSO), elacridar (0.5μM), cabazitaxel (1nM), or a combination of both elacridar and cabazitaxel for 72 hours. Whole cell lysates were then prepared and subjected to western blot analysis using indicated antibodies. Tubulin served as a loading control. c-PARP = cleaved-PARP, C = control (DMSO) treatment, Elac = elacridar, CTX = cabazitaxel. All data is presented as percent of control mean ± standard deviation. * = p-value ≤ 0.05.

CYT997 inhibits cellular proliferation in acute myeloid leukemia (AML) cell lines. Cell viability was measured by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in 96-well plates in the presence of increasing concentrations of CYT997 for 24 h.The results represent the mean ?SD of four replicates.

(B) Viability of cells after exposure to 0, 10, or 10,000 nM docetaxel, assessed by calcein-AM staining (green, left panels) and ethidium homodimer-1 (red, middle panels). Right panels show merged images. Scale bars = 100 μm.

Activity of vinorelbine in NSCLC cell lines in cell viability assay. Activity of vinorelbine NCI-H23, NCI-H460, and NCC44 cell lines in a Cell Titer Glo cell viability assay. Cells were treated with increasing drug concentrations from 0-10000 nM. The data are plotted as the mean % of control cells against the corresponding drug concentration.

Microscope image (406) magnification of U937 cells after exposure to SM-TNs. a) Untreated U937 cells. b) U937 cells treated with 200 nM, and 35 nM ODS empty shells. c) U937 cells treated with microcrystalline (free) Taxol prepared by sonicating Taxol in 20%H3PO4/0.8% SDS solution. d) U937 cells treated with 200 nM SM-TN. A SM-TN is seen in the middle of the picture. e) U937 cells treated with 35 nM SMTN.The nanowires are too small to see at this magnification, but their effect on the cells is clearly visible. Scale bar = 10 mm.

for HXO-RB44 cells, IC50 values for VCR were changed in the different SG600 treatment groups. The results are representative of three independent  experiments and of f our replicates in each experiment.

Matrigel invasion assay of H1299 cells treated with SDF-1α or SDF-1α plus Epothilone B prior to 0 or 2 Gy irradiation. After the treatment for 12 h, the H1299 cells that migrated to the bottom surface of the membrane were stained with Giemsa, and the number of migrated cells was calculated manually.

A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). Total cell lysates were probed with the indicated antibodies against Hippo components on Phos-tag SDS-polyacrylamide gels. O and * mark the non-phosphorylated and phosphorylated proteins, respectively.

ABCB1 functional inhibition using elacridar re-sensitizes TaxR and DU145-DTXR cells to cabazitaxel treatment. A. TaxR and DU145-DTXR cells were subjected to cell growth assays using either vehicle (DMSO), elacridar (0.5μM), cabazitaxel (1nM), or a combination of elacridar and cabazitaxel. Cells were counted 72 hours post-treatment. B. TaxR and DU145-DTXR cells were treated with either vehicle (DMSO), elacridar (0.5μM), cabazitaxel (1nM), or a combination of both elacridar and cabazitaxel for 72 hours. Whole cell lysates were then prepared and subjected to western blot analysis using indicated antibodies. Tubulin served as a loading control. c-PARP = cleaved-PARP, C = control (DMSO) treatment, Elac = elacridar, CTX = cabazitaxel. All data is presented as percent of control mean ± standard deviation. * = p-value ≤ 0.05.

CYT997 inhibits cellular proliferation in acute myeloid leukemia (AML) cell lines. Cell viability was measured by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in 96-well plates in the presence of increasing concentrations of CYT997 for 24 h.The results represent the mean ?SD of four replicates.

(B) Viability of cells after exposure to 0, 10, or 10,000 nM docetaxel, assessed by calcein-AM staining (green, left panels) and ethidium homodimer-1 (red, middle panels). Right panels show merged images. Scale bars = 100 μm.

Activity of vinorelbine in NSCLC cell lines in cell viability assay. Activity of vinorelbine NCI-H23, NCI-H460, and NCC44 cell lines in a Cell Titer Glo cell viability assay. Cells were treated with increasing drug concentrations from 0-10000 nM. The data are plotted as the mean % of control cells against the corresponding drug concentration.