外源性肌醇5′磷酸酶对K562细胞增殖及凋亡的影响

杨琳; 罗建民; 杜行严; 杨敬慈; 刘晓军; 温树鹏; 成志勇

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外源性肌醇5′磷酸酶对K562细胞增殖及凋亡的影响

论著 | 更新时间：2026-01-09

- 外源性肌醇5′磷酸酶对K562细胞增殖及凋亡的影响
- Effects of exogenous SHIP expression on cell growth and apoptosis of K562 cells
- 陆军军医大学学报 2009年31卷第15期页码：1467-1470
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  中图分类号： R394.2;R730.231;R733.71
- 纸质出版：2009
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杨琳,罗建民,杜行严,杨敬慈,刘晓军,温树鹏,成志勇.外源性肌醇5′磷酸酶对K562细胞增殖及凋亡的影响[J].陆军军医大学学报(原第三军医大学学报),2009,31(15):1467-1470.

　YANG Lin,LUO Jian-min,DU Xing-yan,YANG Jing-ci,LIU Xiao-jun,WEN Shu-peng,CHENG Zhi-yong.Effects of exogenous SHIP expression on cell growth and apoptosis of K562 cells[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(15):1467-1470.
杨琳,罗建民,杜行严,杨敬慈,刘晓军,温树鹏,成志勇.外源性肌醇5′磷酸酶对K562细胞增殖及凋亡的影响[J].陆军军医大学学报(原第三军医大学学报),2009,31(15):1467-1470. DOI：

　YANG Lin,LUO Jian-min,DU Xing-yan,YANG Jing-ci,LIU Xiao-jun,WEN Shu-peng,CHENG Zhi-yong.Effects of exogenous SHIP expression on cell growth and apoptosis of K562 cells[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(15):1467-1470. DOI：

摘要

目的通过慢病毒载体介导外源性5′肌醇磷酸酶（SH2 domain contaihing inositol 5′-phosphatase

SHIP）基因转染K562细胞，探讨ship基因对K562细胞生长增殖的影响。方法以白血病细胞株K562为研究对象，将携带ship基因的慢病毒感染K562细胞，FQ-PCR方法检测ship转录水平，Western blot方法检测转染后SHIP蛋白表达变化；比较ship基因表达前后细胞增殖、形态的变化。结果 FQ-PCR和Western blot结果显示，携带ship基因的慢病毒载体pReceiver-Lv31能高效转染K562细胞，阳性率(74.6±5.8)%；细胞生长曲线显示SHIP可显著抑制K562细胞生长，抑制率(35.0±3.1)%；集落形成实验显示SHIP能显著抑制K562细胞集落形成能力[K562/SHIP组集落形成率(36.7±7.1)%，K562/FIV组为(77.7±6.3)%，(P＜0.05)]；细胞形态观察发现凋亡增加，TUNEL法证实SHIP蛋白促进细胞凋亡。结论外源性ship基因表达抑制白血病细胞系K562的增殖活性，并促进其凋亡。

Abstract

Objective To investigate the biological function of SH2 domain containing inositol 5’-phosphatase (ship) gene in cell growth and proliferation. K562 cells by lentiviral vector mediated ship. Methods Exogenous ship gene was delivered into K562 cells by lentiviral vector-based viral infection. SHIP expression was determined by Western blot. Transcription of ship was examined by FQ-PCR. Changes in cell morphology

cell growth

cell apoptosis after SHIP expression were observed. Results FQ-PCR and Western blot demonstrated successful SHIP expression in K562 cells. SHIP protein inhibited the growth of K562 cells [inhibition rate=(35.0±3.1)%] and their colony forming capacity [K562/SHIP group (36.7±7.1)% vs K562/FIV group (77.7±6.3)%

P＜0.05]. Morphological observation showed enhanced cell apoptosis. TUNEL confirmed the enhanced cell apoptosis by SHIP protein. Conclusion ship gene has the potential ability to inhibit leukemic cell proliferation but enhance cell apoptosis.

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