Basic HTML Version
癌症与分子诊断研究
(
网络版
), 2012
年
,
第
1
卷
,
第
3
篇，第
12
-
16
页
Aizheng Yu Fenzi Zhenduan Yanjiu (Online), 2012, Vol.1 No.3, 12
-
16
http://cmdr.5th.sophiapublisher.com
12
研究报告
Research Report
结晶型硫化镍通过自噬途径诱导
16HBE
细胞恶性转化癌变
张岚
1
,
杨磊
2
,
吕嘉春
2
1
广州医学院医学遗传与细胞生物学教研室
,
广州
, 510182;
2
广州医学院化学致癌研究所
,
广州
, 510182
通讯作者
: jiachunlu@163.com;
作者
癌症与分子诊断研究
, 2012
年
,
第
1
卷
,
第
3
篇
doi: 10.5376/cmdr.cn.2012.01.0003
收稿日期：
2012
年
03
月
12
日
接受日期：
2012
年
06
月
28
日
发表日期：
2012
年
07
月
12
日
本文首次发表在《基因组学与应用生物学》
(2012
年第
31
卷第
3
期
222-225
页
)
上。现依据版权所有人授权的许可协议，采用
Creative Commons
Attribution License
协议对其进行授权，再次发表与传播。只要对原作有恰当的引用
,
版权所有人允许并同意第三方无条件的使用与传播。
建议最佳引用格式：
引用格式
(
中文
)
：
张岚等
, 2012,
结晶型硫化镍通过自噬途径诱导
16HBE
细胞恶性转化癌变
,
癌症与分子诊断研究
(online) Vol.1 No.3 pp.12-16 (doi: 10.5376/cmdr.cn.
2012.01.0003)
引用格式
(
英文
)
：
Zhang et al., 2012, Crystalline Nickel Sulfide Induced Malignant Transformation of 16HBE Cells through Autophagic Pathway, Aizheng Yu Fenzi
Zhenduan Yanjiu (Online)Vol.1 No.3 pp.12-16 (doi: 10.5376/cmdr.cn.2012.01.0003)
摘 要
镍化合物广泛存在于人类职业环境中，是人类发生肺癌的主要危险因素。我们前期研究已证实金属毒物结晶型硫化
镍
(NiS)
的暴露是发生肺癌的重要病因，但具体的致癌机制仍未明了。本研究利用前期建立的结晶型
NiS
恶性转化人支气管
上皮细胞的细胞模型，首次采用激光共聚焦扫描显微镜成像技术，在无损伤状态下，实时观测恶性转化细胞
(16HBE-T)
和正常细胞
(16HBE-N)
中自噬体标记蛋白
GFP-LC3
的荧光强度及定位，并利用
Western Blotting
技术检测细胞内自噬信号通路关键效应
分子的表达。共聚焦实验结果表明：
16HBE-T
细胞与
16HBE-N
细胞相比，
GFP-LC3
蛋白的点状聚集明显减少，经测量只有
16HBE-N
细胞的
1/3
左右，表明自噬水平下降；
Western Blotting
检测发现：
mTOR
激酶活性上升，
Beclin 1
表达下降。上述结
果证明，结晶型
NiS
可通过多个自噬途径参与诱导
16HBE
细胞恶性转化的癌变过程，将为预防和治疗肺癌提供重要信息。
关键词
结晶型硫化镍
;
人支气管上皮细胞
;
肺癌
;
自噬
;
自噬体标记蛋白
GFP-LC3; mTOR
激酶
; Beclin 1
Crystalline Nickel Sulfide Induced Malignant Transformation of 16HBE Cells
through Autophagic Pathway
Zhang Lan
1
, Yang Lei
2
, Lv Jiachun
2
1 Department of Medical Genetics and Cell Biology, School of Basic Science, Guangzhou Medical College, Guangzhou, 510182;
2 Institute for Chemical Carcinogenesis, Guangzhou Medical College, Guangzhou, 510182
Corresponding author: jiachunlu@163.com;
Authors
Abstract
Nickel compounds, which widely exist in the environment of human occupation, are the major risk factor for human lung
cancer. Our previous studies had confirmed that exposure to toxic, metallic crystalline nickel sulfide (NiS) was an important cause of
lung cancer, but the concrete carcinogenic mechanism is still unclear. In this study, we used the previously established human
bronchial epithelial (16HBE-T) cells malignant transformation model, which was induced by crystalline NiS. For the first time,
fluorescence intensity and position of the GFP-LC3 protein in malignant transformed (16HBE-T) cells and normal cell (16HBE-N),
were real-time monitored with the technique of confocal laser scanning microscopy imaging without damaging the condition.
Moreover, we used Western Blotting to detect the intracellular autophagic signal which is expressed by key effective molecule
pathway. Confocal experimental results showed that: Compared with that of 16HBE-N-cells, the GFP-LC3 protein punctate
aggregation of 16HBE-T cells significantly reduced to the merely 1/3 amount of 16HBE-N-cells, suggesting that autophagy levels
declined. At the same time, it was found that the mTOR kinase activity increased, and that Beclin 1 expression decreased. The above
research result demonstrated that the mechanism of crystalline NiS induced 16HBE cell malignant transformation was through
multiple autophagic pathway and it will provide an important message in the prevention and treatment of lung cancer.
Keywords
Crystalline NiS; 16HBE; Lung cancer; Autophagy; GFP-LC3; mTOR; Beclin 1