KIF11, a plus end-directed kinesin, as a key gene in benzo(a) pyrene-induced non-small cell lung cancer
KIF11, a plus end-directed kinesin, as a key gene in benzo(a) pyrene-induced non-small cell lung cancer
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DOI：
10.1016/j.etap.2021.103775
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发表时间：
2022-01-01
影响因子：
4.3
通讯作者：
Zhang, Liang
中科院分区：
文献类型：
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作者：
Ling, Junjun;Wang, Yuhong;Zhang, Liang
有证据表明，苯并（a）芘二醇-环氧化物（BPDE）可损伤肺细胞，导致癌变，其机制复杂。我们的目的是探索在这个过程中的基因和途径的变化。首先通过数据挖掘筛选出关键基因并进行鉴定，然后通过生物信息学分析和实验方法进行验证。结果表明，共获得106个上调和260个下调的差异表达基因，这些基因在细胞周期、p53信号通路等多种途径中富集。KIF 11被确定为关键基因。肺癌组织中KIF 11的过表达与病理分级、T分期、淋巴结转移有关，提示肺癌预后不良。综上所述，本研究揭示了KIF 11可能是BPDE相关肺癌发生的关键基因，提高了KIF 11作为BPDE诱导的肺癌预防和治疗的靶点的可能性。
Evidence indicates that Benzo(a)pyrenediol-epoxide (BPDE) can damage lung cells, resulting in carcinogenesis with complex mechanisms. We aimed to explore the genes and pathway variations in this process. First, the key gene was screened out and identified through data mining, and then, it was in turn validated by bioinformatics analysis and experimental methods. Consequently, 106 up-regulated and 260 down-regulated differentially expressed genes were yielded, which were enriched in various pathways, such as Cell cycle, and p53 signaling pathway. Then, KIF11 was identified as the key gene. Overexpression of KIF11 in lung cancer had a correlation with advanced pathological grade, advanced T stage, and presence of lymph node metastasis, which predicted poor prognosis. In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.