Interaction Between IGF1 Polymorphisms and the Risk of Acute Lymphoblastic Leukemia in Chinese Children

Bibliographic Details
Title: Interaction Between IGF1 Polymorphisms and the Risk of Acute Lymphoblastic Leukemia in Chinese Children
Authors: Lingling Lu, Feng Wang, Lulu He, Yao Xue, Yaping Wang, Heng Zhang, Liucheng Rong, Meilin Wang, Zhengdong Zhang, Yongjun Fang, Hongjun Miao
Source: Cellular Physiology and Biochemistry, Vol 36, Iss 4, Pp 1346-1358 (2015)
Publisher Information: Cell Physiol Biochem Press GmbH & Co KG, 2015.
Publication Year: 2015
Collection: LCC:Physiology
LCC:Biochemistry
Subject Terms: Acute lymphoblastic leukemia, Gene-environment interaction, IGF1, MicroRNA, Polymorphism, Physiology, QP1-981, Biochemistry, QD415-436
More Details: Background/Aims: IGF1 is a key regulator in cell proliferation and apoptosis, and the 3' un-translated region (3'UTR) of the gene plays an important role in gene expression. For the first time, we explored the relationship between polymorphisms in the IGF1 3'UTR region and the risk of childhood acute lymphoblastic leukemia (ALL). Methods: Questionnaires were applied to collect epidemiological data. The genotypes of IGF1 polymorphisms were tested in a population of 744 ALL patients and 1088 cancer-free controls utilizing Taqman. Cell functional studies included real-time PCR, cell culture and transfection and luciferase assays. Results: We found that rs6214 homozygous AA genotype and rs6218 homozygous CC genotype were significantly associated with increased risk of childhood ALL. In addition, rs6218 CC genotype was associated with increased level of IGF1 mRNA in bone marrow, and the mutation in rs6218 led to aberrant binding capacity of hsa-miR-603 and hsa-miR-3941 in the 3'UTR of IGF1. Conclusion: Polymorphisms of rs6214 and rs6218 in the 3'UTR of IGF1 are associated with childhood ALL susceptibility, and the polymorphism of rs6218 is related with IGF1 expression at mRNA level.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1015-8987
1421-9778
Relation: http://www.karger.com/Article/FullText/430301; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778
DOI: 10.1159/000430301
Access URL: https://doaj.org/article/913b489aeb3f4671a30e564df0460434
Accession Number: edsdoj.913b489aeb3f4671a30e564df0460434
Database: Directory of Open Access Journals
More Details
ISSN:10158987
14219778
DOI:10.1159/000430301
Published in:Cellular Physiology and Biochemistry
Language:English