10-羟基喜树碱对人膀胱癌细胞增殖、侵袭的抑制作用及诱导凋亡的研究

Inhibition of Proliferation,Anti-invasion and Induction of Apoptosis in Bladder Cancer Cells by 10-HCPT

探讨10-羟基喜树碱(10-HCPT)对人膀胱癌细胞T24增殖、侵袭和诱导凋亡的作用.0.25μmol/L和0.50μmol/L10-HCPT处理T24细胞4d后,用细胞增殖抑制试验、软琼脂集落形成试验、侵袭试验、趋化运动试验、黏附试验和组织蛋白酶B活性测定细胞增殖和侵袭能力的变化;药物处理2d后,采用吖啶橙/溴乙啶荧光双染法和末端脱氧核苷酸转移酶介导dUTP-地高辛缺口末端标记法检测细胞凋亡.结果0.25μmol/L和0.50μmol/L10-HCPT分别使T24细胞增殖下降66.1%和74.8%;对细胞侵袭、运动、黏附及组织蛋白酶B分泌均有明显的抑制作用,并使T24细胞凋亡率显著升高,与对照组比较,差异有显著性意义(P<0.05或0.01).提示10-HCPT有抗T24增殖和侵袭作用,并有诱导凋亡的作用.其抗侵袭机制是对侵袭的多个基本环节起抑制作用.

To investigate effects of 10-HCPT o n inhibition of proliferation,anti-invasion and induction of apoptosis in human bladder cancer ce lls line T 24 .After T 24 cells were treated with 0.25μmol /L and 0.50μmol /L 10-HCPT for 4days,the ability of proliferation and invasion were o bserved by the tests of the inhi-bition of proliferation,the colony-formation in soft agar,the invasio n to reconstituted basement membran e,the laminin adhesion,the chemotatic mi gration and the activity of cathepsin B (CB).After T 24 cells were treated with 10-HCPT for 2days,the rate of ap optosis were tested by the methods of acridine orange ethidium bromide fluorescent stain and terminal deox ynucleotide transferase mediated d UTP-digoxin nick-end-labeling.Af ter T 24 cells were treated with 10-HCPT,the proliferation of T 24 cells decreased to 66.1%and 74.8%re spective-ly.The invasion,adhesion and migra tion ability and the secretion of CB w ere significantly reduced.The rate of apoptosis was obviously increased.Difference was significant (P<0.05or 0.01).We conclude that 10-HCPT can inhibit proliferation and invasive ability,and induce apoptosis of T 24 cells.The mechanism of anti-invasion is to inhibit many key points of the in vasion.