中国现代医学杂志Issue(2)：19-23,5.DOI:10.3969/j.issn.1005-8982.2016.02.004
雷帕霉素对人淋巴瘤细胞株Raji细胞增殖抑制与自噬的机制研究
Rapamycin inhibits proliferation and induces autophagy of human Burkitt lymphoma cells
王炜 1殷玉红 1王志彬 1林鹏 1高玉环2
作者信息
- 1. 河北省保定市第一中心医院 血液科，河北 保定 071000
- 2. 河北医科大学第四医院暨河北省肿瘤医院 血液科，河北 石家庄 050011
- 折叠
摘要
Abstract
Objective To investigate the effect of Rapamycin on growth and autophagy of human Burkitt lymphoma cell line Raji cells and the possible mechanism. Methods Effect of Rapamycin in different concen-trations (0, 1, 5, 10, 20, 40, 50 and 100 nmol/L) on proliferation of Raji cells at different time (24, 48 and 72 h) was detected by MTT assay. Apoptosis and cell cycle were analyzed using flow cytometry. The morpho-logical changes were confirmed using transmission electron microscopy. The expression of Beclin1 protein was examined by Western blot technique in the Rapamycin-treated and untreated Raji cells. Results Rapamycin inhibited the proliferation of Raji cells at concentrations higher than 5 nmol/L ( <0.05) and in a dose- and time-dependent manner. After treatment with Rapamycin, the number of cells in S phase and G2/M phase gradually decreased ( <0.05), but that in G0/G1 phase significantly increased in a dose- and time-dependent manner ( <0.05). However, it did not cause evident apoptosis in Raji cells. Using electron microscope, some large autolysosomes and vacuoles were observed in Raji cells treated with 100 nmol/L Rapamycin for 72 h. Raji cells treated with 0, 1, 10 and 100 nmol/L Rapamycin showed a dose-dependent up-regulation of ex-pression of Beclin1 protein, the classic marker for antophagy. Conclusions Rapamycin inhibits Raji cell pro-liferation by cell cycle arrest in G0/G1 phase and induces autophagy.关键词
雷帕霉素/淋巴瘤/细胞增殖/自噬Key words
Rapamycin/lymphoma/proliferation/autophagy分类
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王炜,殷玉红,王志彬,林鹏,高玉环..雷帕霉素对人淋巴瘤细胞株Raji细胞增殖抑制与自噬的机制研究[J].中国现代医学杂志,2016,(2):19-23,5.
