TRMT10C gene polymorphisms confer hepatoblastoma susceptibility: evidence from a seven-center case-control study.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-08-19 eCollection Date: 2024-01-01 DOI:10.7150/jca.98555
Yanfei Liu, Jinhong Zhu, Xianqiang Wang, Wenli Zhang, Yong Li, Zhonghua Yang, Jiao Zhang, Jiwen Cheng, Li Li, Suhong Li, Jing He, Jun Bian
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引用次数: 0

Abstract

N1-methyladenosine (m1A) is a reversible epigenetic modification of RNAs. Aberrant m1A modification levels due to dysregulation of m1A regulators have been observed in multiple cancers. tRNA methyltransferase 10C (TRMT10C) can install m1A in RNAs; however, its role in hepatoblastoma remains unknown. We conducted this study to identify causal polymorphisms in the TRMT10C gene for hepatoblastoma susceptibility in a cohort of Chinese children (313 cases vs. 1446 controls). The genotypes of four potential functional polymorphisms (rs7641261 C>T, rs2303476 T>C, rs4257518 A>G, and rs3762735 C>G) were determined in participants using TaqMan real-time PCR. The associations of these polymorphisms with hepatoblastoma susceptibility were estimated by logistic regression analysis adjusted for age and sex. All four polymorphisms were significantly associated with hepatoblastoma risk. In particular, under the recessive genetic model, these polymorphisms conferred an increased risk of hepatoblastoma: rs7641261 C>T [adjusted odds ratio (OR)=1.64, 95% confidence interval (CI)=1.04-2.58, P=0.033], rs2303476 T>C (adjusted OR=1.87, 95% CI=1.16-3.02, P=0.010), rs4257518 A>G (adjusted OR=1.45, 95% CI=1.09-1.94, P=0.012), and rs3762735 C>G (adjusted OR=3.83, 95% CI=2.15-6.82, P<0.0001). Combined analysis revealed that kids had an increased risk of developing hepatoblastoma if they harbored at least one risk genotype (adjusted OR=1.94, 95% CI=1.48-2.54, P<0.0001). In addition, the combined risk effects of the four SNPs persisted across all the subgroups. We identified four hepatoblastoma susceptibility loci in the TRMT10C gene. Identifying more disease-causing loci may facilitate the development of genetic marker panels to predict individuals' hepatoblastoma predisposition.

TRMT10C 基因多态性赋予肝母细胞瘤易感性:来自七中心病例对照研究的证据。
N1-甲基腺苷(m1A)是 RNA 的一种可逆表观遗传修饰。tRNA甲基转移酶10C(TRMT10C)可在RNA中安装m1A,但它在肝母细胞瘤中的作用尚不清楚。我们在一组中国儿童(313 例病例与 1446 例对照)中进行了这项研究,以确定 TRMT10C 基因中与肝母细胞瘤易感性相关的多态性。研究人员使用 TaqMan 实时 PCR 测定了四个潜在功能性多态性(rs7641261 C>T、rs2303476 T>C、rs4257518 A>G 和 rs3762735 C>G)的基因型。这些多态性与肝母细胞瘤易感性的关系通过逻辑回归分析进行了估计,并对年龄和性别进行了调整。所有四种多态性都与肝母细胞瘤风险有显著相关性。特别是,在隐性遗传模型下,这些多态性会增加肝母细胞瘤的风险:rs7641261 C>T [调整后的几率比(OR)=1.64,95% 置信区间(CI)=1.04-2.58,P=0.033]、rs2303476 T>C(调整后 OR=1.87,95% CI=1.16-3.02,P=0.010)、rs4257518 A>G(调整后 OR=1.45,95% CI=1.09-1.94,P=0.012)和 rs3762735 C>G(调整后 OR=3.83,95% CI=2.15-6.82,PPTRMT10C 基因)。确定更多的致病位点可能有助于开发基因标记板,以预测个体的肝母细胞瘤易感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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