维甲酸对人骨肉瘤细胞抑制增殖和诱导分化的影响  被引量:3

Tretinoin inhibits proliferation and induces differentiation of human osteogenic sarcoma cells

在线阅读下载全文

作  者:丁凡[1] 邵增务[1] 张保龙[1] 刘之川[1] 徐会法[1] 

机构地区:[1]华中科技大学同济医学院附属协和医院骨科,湖北武汉430022

出  处:《临床骨科杂志》2009年第5期561-564,共4页Journal of Clinical Orthopaedics

摘  要:目的探讨维甲酸对人骨肉瘤(HOS)细胞抑制增殖和诱导分化的影响。方法不同浓度的维甲酸作用HOS细胞,采用噻唑蓝法、倒置相差显微镜观察药物对细胞生长的影响并绘制细胞生长曲线;软琼脂集落形成实验观察细胞生长和侵袭能力的变化;流式细胞仪测定细胞周期变化。结果维甲酸可明显抑制HOS细胞增殖,并呈现剂量和时间的依赖性;细胞形态呈明显的良性分化,瘤细胞的软琼脂集落形成率明显降低;维甲酸能够延缓细胞周期G1~S进程,阻滞细胞于G1期。细胞周期测定结果显示:未经诱导物处理的对照组细胞处于G0/G1期的细胞比例为31.19%;经维甲酸处理之后,实验组细胞G0/G1期的细胞比例上升为57.94%。结论维甲酸对HOS细胞有明显的抑制增殖和诱导分化作用。Objective To study the effect of tretinoin on cellular proliferation and differentiation with human osteogenic sarcoma(HOS) cell.Methods HOS cell line was treated with various concentrations of tretinoin in different durations in vitro.Proliferation suppression was observed by MTT method and invert microscope before and after tretinoin treatment,and protracting cell growth curve.The cell growth and invasion ability was measured with the colony-formation rate in soft agar test.Flow cytometry(FCM) was used to investigate the cell cycle.Results Tretinoin significantly inhibited the proliferation of the human osteogenic sarcoma cell in a dose-dependent and time-dependent manner,and the cell underwent morphological differentiation of benign.The colony-formation rate in semi-solid agar was decreased significantly(P〈0.01).Tretinoin delayed cell cycle G1~S progression and induced a G1 cell cycle arrest.Determination of cell cycle showed that:the cells of the control group without inducer in a period G0/G1 ratio of 31.19%;after treating by tretinoin,the ratio of the G0/G1 phase rose to 57.94%.Conclusions Tretinoin can inhibit the proliferation of osteogenic sarcoma cell and lead to benign differentiation.

关 键 词:骨肉瘤 维甲酸 细胞分化 细胞增殖 

分 类 号:R738.1[医药卫生—肿瘤] R986[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象