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The colchicine derivative CT20126 shows a novel microtubule-modulating activity with apoptosis

Kim, Sung-Kuk, Cho, Sang-Min, Kim, Ho, Seok, Heon, Kim, Soon-Ok, Kyu Kwon, Taeg, Chang, Jong-Soo·2013·Experimental & Molecular Medicine
DOI 10.1038/emm.2013.38PMC PMC3641401
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Figure 1 Turbidity-assessed time course of in vitro microtubule assembly. (a) Chemical structures of colchicine and CT20126. (b) Taxol, colchicine or CT20126 (5 nℳ each) were added to tubulin polymerizing buffer containing 0.1 μg μl−1 tubulin and 1 mℳ guanosine-5'-triphosphate (GTP; arrow ‘a'). After the samples were cooled on an ice bath for depolymerization, repolymerization was initiated by increasing the temperature to 37 °C (arrow ‘b'). DMSO, dimethyl sulfoxide. (c) Dose-response effects of CT20126 on microtubule polymerization. Arrows ‘a' and ‘b' indicate the drug treatment and rewarming times, respectively.
Figure 1 Turbidity-assessed time course of in vitro microtubule assembly. (a) Chemical structures of colchicine and CT20126. (b) Taxol, colchicine or CT20126 (5 nℳ each) were added to tubulin polymerizing buffer containing 0.1 μg μl−1 tubulin and 1 mℳ guanosine-5'-triphosphate (GTP; arrow ‘a'). After the samples were cooled on an ice bath for depolymerization, repolymerization was initiated by increasing the temperature to 37 °C (arrow ‘b'). DMSO, dimethyl sulfoxide. (c) Dose-response effects of CT20126 on microtubule polymerization. Arrows ‘a' and ‘b' indicate the drug treatment and rewarming times, respectively.CC BY-NC-ND · PubMed Central
Figure 2 Modulation of cellular microtubules in response to CT20126 treatment. (a) COS-7 cells were cultured in the presence of various concentrations of CT20126 for 40 min at 37 °C and processed for immunocytochemistry. (b) Comparisons of cellular microtubule modulation induced by treatment with CT20126, colchicine or Taxol (5 μℳ each).
Figure 2 Modulation of cellular microtubules in response to CT20126 treatment. (a) COS-7 cells were cultured in the presence of various concentrations of CT20126 for 40 min at 37 °C and processed for immunocytochemistry. (b) Comparisons of cellular microtubule modulation induced by treatment with CT20126, colchicine or Taxol (5 μℳ each).CC BY-NC-ND · PubMed Central
Figure 3 Tubulin acetylation by CT20126. (a) COS-7 cells treated with CT20126 were lysed and immunoblotted with anti-acetylated α-tubulin antibody. (b) The relative intensities of acetylated α-tubulin obtained from the immunoblot in (a).
Figure 3 Tubulin acetylation by CT20126. (a) COS-7 cells treated with CT20126 were lysed and immunoblotted with anti-acetylated α-tubulin antibody. (b) The relative intensities of acetylated α-tubulin obtained from the immunoblot in (a).CC BY-NC-ND · PubMed Central
Figure 4 Effects of CT20126 on cell cycle distribution. (a) Representative flow cytometric analyses of Jurkat T cells treated with CT20126, colchicine or Taxol. Jurkat T cells were incubated with various concentrations of CT20126 for 24 h. The cells were then fixed and stained with propidium iodide and analyzed by flow cytometry. (b) The percentage of apoptosis (sub-G1 population) induced by different concentrations of CT20126, colchicine or Taxol. (c) Cell cycle distributions of Jurkat T cells treated with CT20126, colchicine or Taxol. Jurkat T cells treated with different concentrations of each drug for 24 h were analyzed for cell cycle by flow cytometry, and the portions of cells in each phase of the cell cycle were quantified. The data are shown as the means of three independent experiments±s.d.
Figure 4 Effects of CT20126 on cell cycle distribution. (a) Representative flow cytometric analyses of Jurkat T cells treated with CT20126, colchicine or Taxol. Jurkat T cells were incubated with various concentrations of CT20126 for 24 h. The cells were then fixed and stained with propidium iodide and analyzed by flow cytometry. (b) The percentage of apoptosis (sub-G1 population) induced by different concentrations of CT20126, colchicine or Taxol. (c) Cell cycle distributions of Jurkat T cells treated with CT20126, colchicine or Taxol. Jurkat T cells treated with different concentrations of each drug for 24 h were analyzed for cell cycle by flow cytometry, and the portions of cells in each phase of the cell cycle were quantified. The data are shown as the means of three independent experiments±s.d.CC BY-NC-ND · PubMed Central
Figure 5 The effects of CT20126 on PARP (poly (ADP-ribose) polymerase) and (PLC-γ1 (phospholipase C-γ1)) cleavage. (a) Jurkat T cells were cultured with different concentrations of CT20126 for 24 h at 37 °C, and cell lysates were analyzed by western blotting with an anti-PARP antibody that detected the 85 kDa fragment of cleaved PARP. (b) Time course of PLC-γ1 cleavage. Jurkat T cells were cultured in the presence of 10 nℳ CT20126 for 0, 3, 6, 12 and 24 h, and lysates were analyzed by western blotting for the 60 kDa fragment of cleaved PLC-γ1.
Figure 5 The effects of CT20126 on PARP (poly (ADP-ribose) polymerase) and (PLC-γ1 (phospholipase C-γ1)) cleavage. (a) Jurkat T cells were cultured with different concentrations of CT20126 for 24 h at 37 °C, and cell lysates were analyzed by western blotting with an anti-PARP antibody that detected the 85 kDa fragment of cleaved PARP. (b) Time course of PLC-γ1 cleavage. Jurkat T cells were cultured in the presence of 10 nℳ CT20126 for 0, 3, 6, 12 and 24 h, and lysates were analyzed by western blotting for the 60 kDa fragment of cleaved PLC-γ1.CC BY-NC-ND · PubMed Central

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Citations

Cites

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Metadata

Authors
Kim, S.-K., Cho, S.-M., Kim, H., Seok, H., Kim, S.-O., Kyu Kwon, T., & Chang, J.-S.
Venue
Experimental & Molecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2013-04-19
Volume
45
Issue
4
Pages
e19-e19
ISSN
2092-6413
DOI
10.1038/emm.2013.38
PMC
PMC3641401
Cited by
37
References
1
Language
en
Licence
www.springer.com/tdm (unspecified)

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