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The prognostic value of ADRA1 subfamily genes in gastric carcinoma

Adrenergic receptor α1 (ADRA1) subfamily members, including ADRA1A, ADRA1B and ADRA1D, are understood to participate in cardiac disease and benign prostatic hyperplasia. In addition, adrenergic signals in cell pathways can promote the development of cancer. However, little is understood regarding th...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2019-09, Vol.18 (3), p.3150-3158
Main Authors: Wang, Tingan, Qin, Yuzhou, Lai, Hao, Wei, Weiyuan, Li, Zhao, Yang, Yang, Huang, Mingwei, Chen, Jiansi
Format: Article
Language:English
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Summary:Adrenergic receptor α1 (ADRA1) subfamily members, including ADRA1A, ADRA1B and ADRA1D, are understood to participate in cardiac disease and benign prostatic hyperplasia. In addition, adrenergic signals in cell pathways can promote the development of cancer. However, little is understood regarding the associations between ADRA1 subfamily members and gastric carcinoma (GC). The present study investigated the prognostic value of the ADRA1 subfamily genes in GC. Data from a total of 379 patients with GC were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases. Kaplan-Meier analysis and Cox regression analysis were used to determine associations with overall survival (OS) and to evaluate the median survival time using hazard ratios (HRs) and 95% confidence intervals (CIs). Multivariate survival analysis revealed that low expression levels of ADRA1A (HR, 0.595; 95% CI, 0.426-0.831; adjusted P=0.002) ADRA1B (HR, 0.576; 95% CI, 0.412-0.805; adjusted P=0.001) and ADRA1D (HR, 0.559; 95% CI, 0.398-0.787; adjusted P=0.001) were associated with a favourable OS. Joint-effects analysis demonstrated that combinations of low expression levels of ARDA1A, ARDA1B and ARDA1D were significantly associated with a favourable OS. Overall, the current results suggested that the mRNA expression levels of ARDA1 subfamily members may serve as potential prognostic markers for GC.
ISSN:1792-1074
1792-0981
1792-1082
DOI:10.3892/ol.2019.10660