Oncotarget

Research Papers:

Correlation between protein kinase catalytic subunit alpha-1 gene rs13361707 polymorphism and gastric cancer susceptibility in asian populations

Jianfeng Ni, Nan Shen, Jilei Tang and Kewei Ren _

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Oncotarget. 2017; 8:68354-68364. https://doi.org/10.18632/oncotarget.19355

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Abstract

Jianfeng Ni1,*, Nan Shen2,*, Jilei Tang3 and Kewei Ren4

1Department of Gastroenterology, Tongzhou People’s Hospital of Nantong, Nantong 226300, China

2Department of Clinical Pharmacy, The Affiliated Jiangyin Hospital of Southeast University Medical School, Jiangyin 214400, China

3Department of Orthopedics, Qidong People’s Hospital, Nantong 226200, China

4Department of Orthopedics, The Affiliated Jiangyin Hospital of Southeast University Medical School, Jiangyin 214400, China

*Co-first author

Correspondence to:

Kewei Ren, email: renkeweijy@163.com

Keywords: protein kinase catalytic subunit alpha-1, gastric cancer, polymorphism, risk, meta-analysis

Received: March 13, 2017    Accepted: June 18, 2017    Published: July 18, 2017

ABSTRACT

A single nucleotide polymorphism (SNP) of the protein kinase catalytic subunit alpha-1 gene (PRKAA1) that confers susceptibility to gastric cancer (GC) was identified by genome-wide association in several case-control studies. However, the results remained controversial and ambiguous. Therefore, we performed a larger meta-analysis to confirm this association. We searched the PubMed, Embase, WanFang, and CNKI databases, without any restriction on language, covering all papers published until Feb 22, 2017. Overall, 14 case-control studies with 14,485 cases and 14,792 controls were retrieved based on the search criteria. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to quantify the strength of the association. Publication bias was assessed by Egger’s and Begg’s tests. We found that the PRKAA1 rs13361707 C/T polymorphism had no association with GC risk in any of the pooled genetic models (for example, the T-allele vs. C-allele allelic contrast model yielded the following estimates: OR = 0.87, 95% CI = 0.73–1.05, Pheterogeneity = 0.000). Furthermore, in analyses stratified by either source of control or geographical origin of subjects, a statistically significant inverse relationship was detected between PRKAA1 rs13361707 C/T polymorphism and GC risk. No obvious evidence of publication bias was detected in the pooled meta-analysis. Furthermore, we observed that individuals carrying T-allele (TT or TC) genotypes had a lower expression of PRKAA1. Our present study indicated that PRKAA1 rs13361707 C/T was not significantly associated with GC risk, despite few positive results in the subgroups.


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