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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

Yuan-Yuan Hu1, Guang-Bin Jiang2, Ya-Feng Song3,4, Ai-Ling Zhan5, Cai Deng1, Yu-Ming Niu1, Lan Zhou1,4, Qi-Wen Duan1
  • 1Department of Stomatology, Department of Clinical Oncology, Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
  • 2Department of Radiology, Suizhou Hospital, Hubei University of Medicine, Suizhou Central Hospital, Suizhou 441300, China
  • 3The Personnel Section, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
  • 4Department of Neurology, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China
  • 5Department of Anesthesiology, Central Hospital of Shanghai Songjiang District, Shanghai 201600, China
* Equal contribution
Received: September 10, 2019Accepted: July 6, 2020Published: October 14, 2020
https://doi.org/10.18632/aging.103696

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.

Abstract

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.