首页|DIP2A对肺腺癌的作用机制和药物敏感度分析

DIP2A对肺腺癌的作用机制和药物敏感度分析

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DIP2A对肺腺癌的作用机制和抗癌药物敏感度具有重要临床意义.挖掘TCGA数据库中肺腺癌TPM标准化的表达矩阵,利用生物信息学方法研究DIP2A对肺腺癌(LUAD)的影响.结果显示,DIP2A在LUAD中高表达;差异基因分析结果显示共有 829 个差异基因(DEGs),其中DIP2A高表达组上调基因813 个,下调基因为13 个,GO和KEGG分析表明,这些差异基因涉及翻译活性和miRNAs在癌症中的发生.药物敏感性分析筛选出IC50与DIP2A表达负相关的11 种药物,包括阿法替尼、阿培利司、PIM抑制剂、Dot1l抑制剂、林西替尼、马来酰亚胺类似物、BCL-2 抑制剂、奈拉滨、奥希替尼、索拉非尼以及极光激酶抑制剂.这些药物可能对 DIP2A高表达肺腺癌具有一定的抑制作用.
Mechanism of Action and Drug Sensitivity Analysis of DIP2A in Lung Adenocarcinoma
DIP2A is clinically important for the mechanism of action and anticancer drug sensitivity in lung adenocarcinoma.In this stud-y,we mined the TPM-normalized expression matrix of lung adenocarcinoma in the TCGA database,and investigated the effect of this gene on lung adenocarcinoma(LUAD)using bioinformatics methods.The results showed that DIP2A was highly expressed in LUAD;differential gene analysis showed a total of 829 differential genes(DEGs),of which 813 genes were up-regulated and 13 genes were down-regulated in the DIP2A high-expression group,and GO and KEGG analyses indicated that these differential genes were involved in translational activity and miRNAs in cancer.Drug sensitivity analysis screens 11 drugs with negative correlation between IC50 and DIP2A expression,including afatinib,apelalis,PIM inhibitors,Dot1l inhibitors,lincitinib,maleimide analogs,BCL-2 inhibitors,ne-larabine,ositinib,sorafenib,and aurora kinase inhibitors.These drugs may have some inhibitory effect on DIP2A-overexpressing lung adenocarcinomas.

DIP2Alung adenocarcinomabioinformatics analysisdrug sensitivity analysis

孙诗卓、刘思奇、吕铮、周月、张继旭、芦小单、丁亦男

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长春师范大学生命科学学院,吉林 长春 130032

吉林省人民医院,吉林 长春 130021

DIP2A 肺腺癌 生物信息学分析 药物敏感度分析

吉林省预算内基本建设资金项目吉林省自然科学基金吉林省中医药科技项目吉林省科技厅项目

2023C041-1YDZJ202201ZYTS148202307920210203186SF

2024

长春师范大学学报
长春师范学院

长春师范大学学报

CHSSCD
影响因子:0.312
ISSN:1008-178X
年,卷(期):2024.43(2)
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