Research Paper Volume 12, Issue 19 pp 19060—19072
Association between the pri-miR-26a-1 rs7372209 C>T polymorphism and cancer susceptibility: multivariate analysis and trial sequential analysis
- 1 Department of Stomatology, Department of Clinical Oncology, Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
- 2 Department of Radiology, Suizhou Hospital, Hubei University of Medicine, Suizhou Central Hospital, Suizhou 441300, China
- 3 The Personnel Section, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
- 4 Department of Neurology, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
- 5 Department of Anesthesiology, Central Hospital of Shanghai Songjiang District, Shanghai 201600, China
Received: September 10, 2019 Accepted: July 6, 2020 Published: October 14, 2020https://doi.org/10.18632/aging.103696
How to Cite
Copyright: © 2020 Hu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
MiR-26 has been suggested to play a tumor-suppressive role in cancer development, which could be influenced by the mutate pri-miR-26ª-1. Molecular epidemiological studies have demonstrated some inconsistent associations between pri-miR-26ª-1 rs7372209 C>T polymorphism and cancer risk. We therefore performed this meta-analysis with multivariate statistic method to comprehensively evaluate the associations between rs7372209 C>T polymorphism and cancer risk. Eleven publications involving 6,709 patients and 6,514 controls were identified. Multivariate analysis indicated that the over-dominant genetic model was most likely. Pooled results indicated no significant association in the overall population (CC+TT vs. CT: OR=1.08, 95%CI=0.96-1.22, P=0.20, I2=54.4%), as well as the subgroup analysis according to ethnicity, control source, tumor locations, and HWE status of controls. In addition, heterogeneity, accumulative, sensitivity analysis, publication bias and trial sequential analysis (TSA) were conducted to test the statistical power. Overall, our results indicated that the pri-miR-26a-1 rs7372209 C>T polymorphism may not be a potential risk for cancer development.