摘要
目的:研究克霉唑对结肠癌细胞生长,粘附和侵袭转移中的作用。并初步探讨其机制。方法:用不同浓度的克霉唑加入培养中的结肠癌细胞株CCL229中,观察加药前后细胞生长速度的变化;检测细胞与基质的粘附能力;用细胞分离试验测定细胞的同质粘附性。Boyden小室法检测细胞的侵袭能力;流式细胞光度术检测细胞尿激酶型纤溶原激活剂(Urokinasetypeplasminogenactivator,UPA)表达。结果:药物作用后,CCL229细胞体外增殖能力减弱;在低浓度药物作用时,与基质粘附能力和同质粘附性均无明显变化,高浓度药物作用后,与基质和同质粘附性均下降;体外侵袭实验表明,药物作用后,CCL229细胞穿过基底膜能力减弱;细胞UPA表达量下降。结论:克霉唑使细胞的恶性表型发生变化,可使其侵袭转移能力受到抑制,并呈现剂量依赖性。
Objective: To study the effects
and its mechanism of clotrimazole on colorectal cancer cell line
proliferation,adherence,invasion and metastasis. Methods: Using experiment in vitro,we added
clotrimazole of different concentrations into the medium in which the cells were cultured.The
changes of cell proliferation were observed.Adhesiveness to the extracellular matrix was
detected by MTT.Hemotypic adhesion was investigated by detachment assay and invasiveness
of the cells was observed with Boyden Chamber before and after the drug treatment.The
expresion of UPA(urokinasetype plasminogen activator was measured with flow cytometry.
Results: The growth rate of CCL229 was decreased after clotrimazole treatment;no difference of
the adhesiveness of the cells to extracelular matrix was observed with clotrimazole at low
concentration. While with the high concentrtion,both the adhensiveness to the extracellular
matrix and hemotypic adhesion were decreased.Invasion assay showed that invasiveness of
CCL229 was decreased.Expression of UPA was also decreased. Conclusion: Malignant
phenotype of CCL229 was changed and its invasive ability was inhibited by clotrimazole.in
dosedependent manner.
出处
《癌症》
SCIE
CAS
CSCD
北大核心
1999年第3期253-255,共3页
Chinese Journal of Cancer