Abstract
We assessed the relationship between AGT gene M235T polymorphism and the susceptibility to cancer by performing an updated meta-analysis. This study retrospectively searched related articles in the electronic databases. Afterwards, we determined combined odds ratios (ORs) and related 95% confidence intervals (CIs) by the fixed- or random-effects model. The present meta-analysis enrolled altogether 9 articles. On the whole, the relationship between AGT M235T polymorphism and the cancer risk was not significant among the entire population (TT vs. MM: OR = 1.28, 95%CI = 0.80 − 2.04; TM vs. MM: OR = 0.90, 95%CI = 0.53 − 1.52; recessive model: OR = 1.13, 95%CI = 0.83 − 1.52; dominant model: OR = 0.93, 95%CI = 0.55 − 1.57). Subgroup analysis by ethnicity, cancer type, and study quality for the relationship between the AGT M235T polymorphism and cancer risk showed no significant association. According to findings in the present meta-analysis, AGT M235T polymorphism may not be related to cancer susceptibility.
Highlights
Genetic factors are recognized to exert vital parts in cancer risk, with numerous cancer pathogenesis-related genes being identified as the cancer risk genes [3]
As reported in some studies, the interaction between polymorphisms and environmental factors exerts a vital part in cancer genesis
More and more studies find that Renin-angiotensin system (RAS) affects cell proliferation, inflammation, apoptosis, and tissue angiogenesis
Summary
Cancer greatly affects the global economy and public health. According to statistics, 14 million cancer patients are diagnosed in 2012, and the cancer morbidity is predicted to increase to nearly 22 million in 2030 [1]. The cancer pathogenic mechanism remains largely unclear, and cancer is reported as a complicated condition induced by numerous factors, such as genetic factors, smoking, excessive drinking, chemical dyes, high-calorie diet, or their combination [2]. Renin can release 10 amino acids (aa) in angiotensinogen (AGT) for forming Ang I as well as the great protein (des (Ang I) AGT). Both des (Ang I) AGT and AGT have been recognized as the noninhibitory serpins inhibiting new blood vessel formation [5]. Ang II represents a major RAS active peptide that can promote cell proliferation and new blood vessel formation via angiotensin II type 1 receptor (AGTR1) [6]
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