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. 2010 Jun;101(6):1382-6.
doi: 10.1111/j.1349-7006.2010.01540.x. Epub 2010 Feb 22.

"VSports app下载" Docetaxel suppresses invasiveness of head and neck cancer cells in vitro

Yasunao Kogashiwa  1 , Hiroyuki Sakurai, Toru Kimura, Naoyuki Kohno
Affiliations

Docetaxel suppresses invasiveness of head and neck cancer cells in vitro

"V体育安卓版" Yasunao Kogashiwa et al. Cancer Sci. 2010 Jun.

Abstract

The combination of docetaxel, cisplatin, and fluorouracil significantly enhances the survival of head and neck cancer patients compared to cisplatin and fluorouracil. We hypothesized that docetaxel may affect invasiveness of the head and neck cancer cells in addition to its tumor-killing effect. Two different head and neck cancer cell lines (HEp-2 and Ca9-22) were treated with docetaxel at IC(10) and IC(50) concentrations. Cell migration and invasive growth was evaluated by wound healing assay and three-dimensional (3D) culture of multicellular tumor spheroids, respectively. Expression levels of possible downstream effectors for cell migration/invasiveness were measured by immunoblotting in conditions with or without docetaxel. Docetaxel, but not cisplatin, suppressed filopodia formation compared with no treatment (control) condition VSports手机版. Consistent with this, docetaxel suppressed two-dimensional (2D) cell migration and 3D cell invasion compared with control or cisplatin. Only docetaxel treated cells exhibited thick tubulin bundle and had lower activity of Cdc42, a member of the Rho family of small GTPases. In conclusion, Docetaxel treatment suppressed migration and invasiveness of head and neck cancer cells in vitro, which is likely to be mediated by regulating Cdc42 activity. .

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Figures

Figure 1
Figure 1
Growth curve after 1‐h drug exposure followed by a 96‐h incubation in cisplatin or docetaxel treatment. Control cell growth = 1.0. Each data point represents mean ± SE.
Figure 2
Figure 2
Migration assay at IC10 in two head and neck cancer cell lines. Migration rate compared to control cell migration rate. Each data point represents mean ± SE. **P < 0.001.
Figure 3
Figure 3
Three‐dimensional‐Gel culture of HEp‐2 cell spheroids at IC50 concentration. HEp‐2 cell spheroids were treated with cisplatin or docetaxel at IC50 followed by 96‐h incubation. Bars, 250 μm.
Figure 4
Figure 4
Staining of α‐tubulin (anti‐α‐tubulin), F‐actin (phalloidin), and nucleus (DAPI) in HEp‐2 cells and Ca9‐22 cells treated by cisplatin, docetaxel, or no treatment at IC50. Arrows, thick tubulin bundle; arrow heads, filopodia. Bars, 50 μm.
Figure 5
Figure 5
(a) Colorimetric assay of Cdc42, Rac, and RhoA activity in HEp‐2 cells. The levels of activated Cdc42, Rac, and RhoA in HEp‐2 cells were evaluated immediately after 1 h of indicated treatment. Each data point represents mean ± SE. *P < 0.05, **P < 0.01. (b) Western blot analysis of rho family GTPases. (c) Immunostaining of Cdc42, Rac1, and RhoA in HEp‐2 cells treated by cisplatin, docetaxel, or no treatment at IC10. Nucleus was stained by DAPI. Arrows, Cdc42 localized at plasma membrane of HEp‐2 cells. Bars, 25 μm.
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References (VSports注册入口)

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