摘要
目的:探讨As2O3对人乳腺癌MCF-7细胞和多药耐药MCF-7/ADR细胞生长抑制作用的差异。方法:采用MTT还原法、光镜、电镜和流式细胞术等方法检测As2O3对MCF-7和MCF-7/ADR细胞的生长抑制作用和诱导凋亡的情况。结果:As2O3对MCF-7和MCF-7/ADR细胞均有生长抑制作用,并呈时间剂量依赖关系,96h的IC50值分别为3μmol/L和12.8μmol/L,形态学检测显示其抑制作用主要源于凋亡;在相同作用时间及浓度下,As2O3对MCF-7细胞的抑制率显著高于MCF-7/ADR细胞,起效时间亦早于后者。结论:As2O3能诱导乳腺癌MCF-7和MCF-7/ADR细胞凋亡;MCF-7/ADR细胞虽对As2O3表现耐药,但耐药倍数较低(4.27)。
Objective .To explore the difference between the growth inhibition effect of arsenic trioxide(As2O3)on the human breast cancer MCF 7 and multidrug resistance MCF-7/ADR cell line. Niches MCF - 7 and MCF-7/ADR cell was cultured with 0.5μmol/L~16μmol/L arsenic trioxide in vitro. MTT test was adopted to detect the growth suppression effect of As2O3 in the two cell lines. Apoptosis morphology was studied with light microscope and electron microscope. Apoptosis ratio was analysed with flow cytometry. Results :As2O3 could inhibit the proliferation of the MCF-7 and MCF - 7/ADR cell line, especially that of 2μmol/L~ 16μmol/L, and the effect was dose - and - time dependent. The IC50 at 96h was 3.0μmol/L for MCF-7 and 12.8μmol/L for MCF - 7/ADR. Cell morphology and flow cytometry revealed the growth suppression was caused mainly by apoptosis rather than necrosis; however, to obtain the same inhibitory level, MCF-7/ADR cell required higher concentration of As2O3 and longer processing time. Conclusion :As2O3 can inhibit the proliferation in MCF- 7/ADR cell as well as MCF- 7 cell,though MCF- 7/ADR cell is tolerant to As2O3 ,but the tolerance is at a low level.
出处
《重庆医科大学学报》
CAS
CSCD
2005年第4期570-573,共4页
Journal of Chongqing Medical University