| Title |
Functional polymorphisms in NFκB1/IκBα predict risks of chronic obstructive pulmonary disease and lung cancer in Chinese
|
|---|---|
| Published in |
Human Genetics, January 2013
|
| DOI | 10.1007/s00439-013-1264-9 |
| Pubmed ID | |
| Authors |
Dongsheng Huang, Lei Yang, Yehua Liu, Yumin Zhou, Yuan Guo, Mingan Pan, Yunnan Wang, Yigang Tan, Haibo Zhong, Min Hu, Wenju Lu, Weidong Ji, Jian Wang, Pixin Ran, Nanshan Zhong, Yifeng Zhou, Jiachun Lu |
| Abstract |
Lung inflammation is the major pathogenetic feature for both chronic obstructive pulmonary disease (COPD) and lung cancer. The nuclear factor-kappa B (NFκB) and its inhibitor (IκB) play crucial roles in inflammatory. Here, we tested the hypothesis that single nucleotide polymorphisms (SNPs) in NFκB/IκB confer consistent risks for COPD and lung cancer. Four putative functional SNPs (NFκB1: -94del>insATTG; NFκB2: -2966G>A; IκBα: -826C>T, 2758G>A) were analyzed in southern and validated in eastern Chineses to test their associations with COPD risk in 1,511 COPD patients and 1,677 normal lung function controls, as well as lung cancer risk in 1,559 lung cancer cases and 1,679 cancer-free controls. We found that the -94ins ATTG variants (ins/del + ins/ins) in NFκB1 conferred an increased risk of COPD (OR 1.27, 95% CI 1.06-1.52) and promoted COPD progression by accelerating annual FEV1 decline (P = 0.015). The 2758AA variant in IκBα had an increased risk of lung cancer (OR 1.53, 95% CI 1.30-1.80) by decreasing IκBα expression due to the modulation of microRNA hsa-miR-449a but not hsa-miR-34b. Furthermore, both adverse genotypes exerted effect on increasing lung cancer risk in individuals with pre-existing COPD, while the -94del>insATTG did not in those without pre-existing COPD. However, no significant association with COPD or lung cancer was observed for -2966G>A and -826C>T. Our data suggested a common susceptible mechanism of inflammation in lung induced by genetic variants in NFκB1 (-94del>ins ATTG) or IκBα (2758G>A) to predict risk of COPD or lung cancer. |
Mendeley readers
The data shown below were compiled from readership statistics for 29 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 29 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 8 | 28% |
| Student > Ph. D. Student | 4 | 14% |
| Student > Master | 3 | 10% |
| Student > Bachelor | 2 | 7% |
| Student > Doctoral Student | 1 | 3% |
| Other | 6 | 21% |
| Unknown | 5 | 17% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 7 | 24% |
| Agricultural and Biological Sciences | 5 | 17% |
| Biochemistry, Genetics and Molecular Biology | 3 | 10% |
| Nursing and Health Professions | 2 | 7% |
| Computer Science | 2 | 7% |
| Other | 5 | 17% |
| Unknown | 5 | 17% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 May 2013.
All research outputs
#20,194,150
of 22,711,242 outputs
Outputs from Human Genetics
#2,813
of 2,950 outputs
Outputs of similar age
#252,287
of 285,030 outputs
Outputs of similar age from Human Genetics
#12
of 13 outputs
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