The expression of ADAM23 and its correlation with promoter methylation in non‐small‐cell lung carcinoma

甲基化 免疫组织化学 肺癌 化学 DNA甲基化 分子生物学 癌症研究 发起人 基因表达 病理 生物 基因 免疫学 医学 生物化学
作者
Chunyan Hu,Hui Lv,Guoqing Pan,Hui-qiu Cao,Zhenghao Deng,Chuanyu Hu,Jifang Wen,Jianhua Zhou
出处
期刊:International Journal of Experimental Pathology [Wiley]
卷期号:92 (5): 333-339 被引量:17
标识
DOI:10.1111/j.1365-2613.2011.00766.x
摘要

Summary ADAM23, a member of a disintegrin and metalloprotease (ADAM) family, has been reported to be expressed in several types of tumours. The exact role of ADAM23 and the possible mechanisms in which it is involved in non‐small‐cell lung carcinoma (NSCLC) remains unclear. Therefore, this study was designed to explore the expression of ADAM23 and its correlation with promoter methylation in NSCLC. Immunohistochemistry and RT‐PCR together with Western blotting methods were used to analyse the expression of ADAM23 in 52 cancer tissue samples and eight benign pulmonary lesions as well as four cell lines. The methylated status of ADAM23 gene was determined with methylation‐specific PCR (MSP). The results of immunohistochemistry showed that the expression of ADAM23 protein was lower in NSCLC than that in corresponding normal tissues and benign pulmonary lesions (38.5% vs. 86.5% and 87.5%, P < 0.05), and decreased as NSCLC progressed. Meanwhile, methylation of ADAM23 gene was observed in 21 of 52 NSCLC tissues (40.4%), much higher than that of adjacent normal tissues (7.6%) and benign pulmonary lesions (0/8). In the cancer tissues of ADAM23‐negative samples, the rate of ADAM23 gene methylation was 50.3% (17/32). ADAM23 expression and its promoter methylation were negatively associated ( r = −0.328, P = 0.017). Moreover, weak expression of ADAM23 in methylated cancer cells increased after treatment with 5‐aza‐2′‐deoxycytidine (5‐Aza‐2′‐dC), confirming that methylation was responsible for the gene downregulation. Our results demonstrate that the expression level of ADAM23 is likely to be involved in the progression of NSCLC and its downregulation is probably correlated with promoter methylation. These findings may provide potential diagnostic and prognostic information about NSCLC.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
赘婿应助阿航采纳,获得10
刚刚
LL完成签到,获得积分10
2秒前
flysteven92完成签到 ,获得积分10
2秒前
酷波er应助xc采纳,获得10
3秒前
5秒前
liss发布了新的文献求助10
6秒前
LL完成签到,获得积分10
7秒前
淡淡的白羊完成签到 ,获得积分10
8秒前
9秒前
DUBUYINKE完成签到,获得积分10
9秒前
9秒前
天雨流芳完成签到 ,获得积分10
10秒前
何公主完成签到,获得积分10
12秒前
科研通AI6.3应助小c采纳,获得10
12秒前
夜绒枭完成签到 ,获得积分10
12秒前
云为翳完成签到,获得积分10
13秒前
短腿小柯基完成签到 ,获得积分10
13秒前
13秒前
危机的夏兰完成签到,获得积分10
15秒前
汉堡包应助xc采纳,获得10
15秒前
16秒前
DoctorXu完成签到,获得积分10
17秒前
heavennew完成签到,获得积分10
17秒前
核桃发布了新的文献求助30
20秒前
20秒前
smalldesk完成签到,获得积分10
21秒前
21秒前
SNE完成签到,获得积分10
25秒前
七页禾完成签到,获得积分10
25秒前
Owen应助yy采纳,获得10
25秒前
炸鸡大王完成签到,获得积分10
26秒前
阿莫西林胶囊完成签到,获得积分10
27秒前
杨洋完成签到 ,获得积分10
27秒前
27秒前
28秒前
dde完成签到,获得积分10
30秒前
Largequail发布了新的文献求助10
32秒前
科研通AI6.3应助直率愫采纳,获得10
32秒前
CHONGMING发布了新的文献求助10
32秒前
34秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Social Cognition: Understanding People and Events 1000
Polymorphism and polytypism in crystals 1000
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6029417
求助须知:如何正确求助?哪些是违规求助? 7699913
关于积分的说明 16190209
捐赠科研通 5176651
什么是DOI,文献DOI怎么找? 2770197
邀请新用户注册赠送积分活动 1753495
关于科研通互助平台的介绍 1639245