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第43卷第7期                           南京医科大学学报(自然科学版)
                  2023年7月                   Journal of Nanjing Medical University(Natural Sciences)     ·917 ·


               ·基础研究·

                糖基化基因B4GALT5在胰腺癌恶性进展中的作用



                刘雪昂 ,时       坚 ,胡 冉 ,朱 岩 ,马文静 ,朱 毅               1,2*
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                南京医科大学第一附属医院胰腺中心,江苏                 南京   210029;南京医科大学胰腺研究所,江苏             南京   210029;南京医科大
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                学第一附属医院公共实验中心,病理科,江苏 南京                   210029
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               [摘   要] 目的:基于糖基化基因集在TCGA⁃GTEx联合公共数据库中挖掘与胰腺癌发生风险和不良预后显著相关的基因,利
                用本中心的组织样本和体外实验进行验证。方法:通过公共数据库筛选到与胰腺癌发生风险和不良预后相关的糖基化基因
                B4GALT5,使用本中心有临床与预后信息的组织样本进行验证。构建B4GALT5干扰和过表达的胰腺癌细胞系,通过CCK⁃8、
                细胞划痕和Transwell侵袭实验观察B4GALT5在体外对胰腺癌细胞恶性生物学行为的作用。结果:胰腺癌组织中B4GALT5的
                表达显著高于正常组织,并且B4GALT5的表达量增高与胰腺癌发生风险和不良预后呈显著正相关,与CD4 T细胞和自然杀伤
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                T细胞浸润呈负相关。B4GALT5在胰腺癌细胞的体外增殖、运动、浸润过程中起促进作用。结论:糖基化基因B4GALT5有促
                进胰腺癌恶性进展的作用,可能作为新的生物标志物预测胰腺癌发生风险与不良预后。
               [关键词] 胰腺癌;糖基化;B4GALT5;糖基转移酶;生存分析
               [中图分类号] R735.9                    [文献标志码] A                      [文章编号] 1007⁃4368(2023)07⁃917⁃11
                doi:10.7655/NYDXBNS20230704


                Role of glycosylation gene B4GALT5 in malignant progression of pancreatic cancer

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                LIU Xue’ang ,SHI Jian ,HU Ran ,ZHU Yan ,MA Wenjing ,ZHU Yi  1,2*
                Pancreas Centre,the First Affiliated Hospital of Nanjing Medical University,Nanjing 210029;Pancreas Institute,
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                Nanjing Medical University,Nanjing 210029;Public Laboratory Center,Department of Pathology,the First
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                Affiliated Hospital of Nanjing Medical University,Nanjing 210029,China
               [Abstract] Objective:Based on the glycosylation related gene set,the TCGA⁃GTEx joint public database was used to identify genes
                significantly related to the occurrence and poor prognosis of pancreatic cancer,and the tissue samples of our center and in vitro
                experiments were used for verification. Methods:The glycosylation gene B4GALT5 related to the risk and poor prognosis of pancreatic
                cancer was screened through the public database,and was verified using the tissue samples of our center with clinical and prognostic
                information. We constructed pancreatic cancer cell lines with B4GALT5 interference and overexpression,and observed the effects of
                B4GALT5 on the malignant biological behavior of pancreatic cancer cells in vitro through CCK⁃8,wound healing,transwell invasion
                experiments. Results:The expression of B4GALT5 in pancreatic cancer tissue was significantly higher than that in normal pancreatic
                tissue. The increased expression of B4GALT5 was positively correlated with the risk and poor prognosis of pancreatic cancer,and
                negatively correlated with the infiltration of CD4 T cells and NK T cells. B4GALT5 played a role in exacerbating the proliferation,
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                movement and invasion of pancreatic cancer cells in vitro. Conclusion:The glycosylation gene B4GALT5 can promote the malignant
                progression of pancreatic cancer,and may be used as a new biomarker to indicate the risk and poor prognosis of pancreatic cancer.
               [Key words] pancreatic cancer;glycosylation;B4GALT5;glycosyltransferase;survival analysis
                                                                           [J Nanjing Med Univ,2023,43(07):917⁃926,944]




                                                                      胰腺癌(pancreatic cancer,PC)是一种高度侵袭
                                                                  性和致命性的恶性肿瘤,是目前癌症死亡的第三大
                                                                                          [2]
                                                                      [1]
               [基金项目] 江苏省“六大人才高峰”人才项目(WSW⁃032)                    原因 ,远处转移超过50% ,对放疗、化疗不敏感,
                ∗                                                 只有 15%~20%的患者能从手术中获益,5 年生存率
                通信作者(Corresponding author),E⁃mail:zhuyijssry@126.com
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