Genetic variants in glycosylation pathways are associated with colorectal cancer risk.

IF 3.3 3区 医学 Q2 ONCOLOGY
Huiyu Wang, Hanchi Wu, Xiaoting He, Hao Wang, Junying Xu, Junli Ding, Shuwei Li, Dong Hua, Meilin Wang
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引用次数: 0

Abstract

The glycosylation pathway serves as a vital regulatory mechanism in colorectal cancer. However, how genetic variants in these pathways may affect the risk of colorectal cancer is still unknown. To examine the relationships between the risk of colorectal cancer and the presence of selected single-nucleotide polymorphisms (SNPs), 1,150 patients and 1,342 controls were included in this case‒control study. We found that GALNT2 rs76000797 and rs11576324, GALNT6 rs67726586, FUT8 rs117497405, FUT2 rs111311275 and B4GALT5 rs6125695 were strongly correlated with the risk of colorectal cancer. Moreover, rs111311275 exhibited an expression quantitative trait locus effect on FUT2 in colorectal cancer tissues, which could increase the risk of colorectal cancer by influencing FUT2 expression. GEPIA research and microarray data revealed that FUT2 expression was higher in colorectal cancer tissues than in normal tissues and that individuals with colon cancer with high expression of FUT2 had longer overall survival times. Our study highlights the significant impact of genetic variants on glycosylation pathways and offers novel insights into potential biomarkers for colorectal cancer risk.

糖基化途径中的遗传变异与结直肠癌风险相关。
糖基化途径是结直肠癌的重要调控机制。然而,这些途径中的遗传变异如何影响结直肠癌的风险仍然未知。为了研究结直肠癌风险与所选单核苷酸多态性(snp)之间的关系,本病例对照研究纳入了1150例患者和1342例对照。我们发现GALNT2 rs76000797和rs11576324、GALNT6 rs67726586、FUT8 rs117497405、FUT2 rs111311275和B4GALT5 rs6125695与结直肠癌的发生风险密切相关。此外,rs111311275在结直肠癌组织中对FUT2表现出表达数量性状位点效应,可能通过影响FUT2表达而增加结直肠癌的发生风险。GEPIA研究和微阵列数据显示,FUT2在结直肠癌组织中的表达高于正常组织,并且FUT2高表达的结肠癌患者的总生存时间更长。我们的研究强调了基因变异对糖基化途径的重要影响,并为结直肠癌风险的潜在生物标志物提供了新的见解。
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
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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