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[BCSC-1基因异位表达导致鼻咽癌CNE-2L2细胞黏附增强及细胞周期阻滞]

[Ectopic expression of BCSC-1 gene results in enhancement of adhesion and cell cycling blockade of nasopharyngeal carcinoma CNE-2L2 cell].

作者信息

Chen Shuang-ling, Zhou Yi-qun, Tian Yun, Ju Ji-yu, Liu Yin, Zhu Li-ping

机构信息

Department of Immunology, Institute of Basic Medical Sciences, CAMS and PUMC, Beijing 100005, China.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2007 Aug;29(4):533-7.

Abstract

OBJECTIVE

To study mechanisms of reduction of the malignant activities of human naso-pharyngeal carcinoma cell CNE-2L2 induced by ectopic expression of BCSC-1 gene.

METHODS

DNA was stained with propidium iodide and assayed upon a flow cytometer. Chromosomes were stained with Hoechest 33258. Adhesion of CNE-2L2 cells was detected by cell aggregation test. Protein expression on CNE-2L2 cells was examined by Western blot.

RESULTS

Cell cycle analysis showed that the percentage of CNE-2L2 cells was 55.1%, 43.4%, and 39.4% in G0/G1 phase, 25.2%, 28.7%, and 30.9% in S phase, and 19.7%, 27.9%, and 29.7% in G2/M phase for the cell with ectopic expression of BCSC-1 gene, wild type cell (W cells), and the cell transduced with the mock (M cell). Many mitotic cells were found in W cells and M cells. In contrast, almost no mitotic cell was observed in the cells with ectopic expression of BCSC-1 gene. Ectopic BCSC-1 expression resulted in cell aggregation, enhanced expression of E-cadherin, cx-catenin, and p53.

CONCLUSIONS

Ectopic BCSC-1 expression causes enhancement of adhesion of CNE-2L2 cells associated with enhanced expression of E-cadherin and alpha-catenin, arrest of cell in G1 phase, which may be associated with enhanced expression of p53. These alteration may play a role in the reduction of malignant activities of the cells with ectopic expression of BCSC-1 gene.

摘要

目的

研究BCSC-1基因异位表达诱导人鼻咽癌CNE-2L2细胞恶性活性降低的机制。

方法

用碘化丙啶对DNA进行染色,并在流式细胞仪上进行检测。用Hoechest 33258对染色体进行染色。通过细胞聚集试验检测CNE-2L2细胞的黏附情况。用蛋白质印迹法检测CNE-2L2细胞上的蛋白质表达。

结果

细胞周期分析显示,BCSC-1基因异位表达的细胞、野生型细胞(W细胞)和用空载体转导的细胞(M细胞)在G0/G1期的比例分别为55.1%、43.4%和39.4%,在S期的比例分别为25.2%、28.7%和30.9%,在G2/M期的比例分别为19.7%、27.9%和29.7%。在W细胞和M细胞中发现许多有丝分裂细胞。相比之下,在BCSC-1基因异位表达的细胞中几乎未观察到有丝分裂细胞。BCSC-1基因异位表达导致细胞聚集,E-钙黏蛋白、α-连环蛋白和p53的表达增强。

结论

BCSC-1基因异位表达导致CNE-2L2细胞黏附增强,与E-钙黏蛋白和α-连环蛋白表达增强相关,细胞停滞在G1期,这可能与p53表达增强有关。这些改变可能在BCSC-1基因异位表达细胞的恶性活性降低中起作用。

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