细胞周期蛋白B2(CCNB2)属于B型细胞周期家族蛋白,它位于染色体15q22上,并与细胞周期蛋白依赖性激酶(CDK)结合以调节其活性。在这项研究中,收集了103个与肺癌(LC)和缺血性脑卒中(CIS)的所有亚型相关的高通量数据集以及CCNB2表达数据。反映表达状态的标准平均差(SMD)和概括接受者工作特征(SROC)的分析表明,LC和CIS中CCNB2的显着上调(肺腺癌:SMD=1.40,95CI[0.98-1.83],SROC=0.92,95CI[0.89-0.94]。肺鳞状细胞癌:SMD=2.56,95CI[1.64-3.48]。SROC=0.97,95CI[0.95-0.98]。肺小细胞癌:SMD=3.01,95CI[2.01-4.01]。SROC=0.98,95CI[0.97-0.99]。CIS:SMD=0.29,95CI[0.05-0.53],SROC=0.68,95CI[0.63-0.71])。同时,蛋白质-蛋白质相互作用(PPI)分析表明,CCNB2是CIS和LC中交叉高表达基因的中心分子。通过多尺度嵌入基因共表达网络分析(MEGENA),获得了包括76个基因的CIS基因模块,CCNB2模块基因的功能富集分析表明,CCNB2可能参与CIS的形成和CIS引起的组织损伤的过程,如“细胞周期,蛋白激酶活性,“和”鞘糖脂生物合成。\"之后,通过单细胞RNA-seq分析,发现CCNB2在脑类器官中的GABA能神经元以及在LUAD中表达增殖分子的T细胞上上调。同时,CCNB2的表达与TOP2A相似,作为细胞增殖的模块标志物在细胞群中分布。这些发现有助于LC相关CIS的发病机制和CIS损伤后的神经元修复。
Cyclin B2 (CCNB2) belongs to type B cell cycle family protein, which is located on chromosome 15q22, and it binds to cyclin-dependent kinases (CDKs) to regulate their activities. In this
study, 103 high-throughput datasets related to all subtypes of lung cancer (LC) and cerebral ischemic stroke (CIS) with the data of CCNB2 expression were collected. The analysis of standard mean deviation (SMD) and summary receiver operating characteristic (SROC) reflecting expression status demonstrated significant up-regulation of CCNB2 in LC and CIS (Lung adenocarcinoma: SMD = 1.40, 95%CI [0.98-1.83], SROC = 0.92, 95%CI [0.89-0.94]. Lung squamous cell carcinoma: SMD = 2.56, 95%CI [1.64-3.48]. SROC = 0.97, 95%CI [0.95-0.98]. Lung small cell carcinoma: SMD = 3.01, 95%CI [2.01-4.01]. SROC = 0.98, 95%CI [0.97-0.99]. CIS: SMD = 0.29, 95%CI [0.05-0.53], SROC = 0.68, 95%CI [0.63-0.71]). Simultaneously, protein-protein interaction (PPI) analysis indicated that CCNB2 is the hub molecule of crossed high-expressed genes in CIS and LC. Through Multiscale embedded gene co-expression network analysis (MEGENA), a gene module of CIS including 76 genes was obtained and function enrichment analysis of the CCNB2 module genes implied that CCNB2 may participate in the processes in the formation of CIS and tissue damage caused by CIS, such as \"cell cycle,\" \"protein kinase activity,\" and \"glycosphingolipid biosynthesis.\" Afterward, via single-cell RNA-seq analysis, CCNB2 was found up-regulated on GABAergic neurons in brain organoids as well as T cells expressing proliferative molecules in LUAD. Concurrently, the expression of CCNB2 distributed similarly to TOP2A as a module marker of cell proliferation in cell cluster. These findings can help in the field of the pathogenesis of LC-related CIS and neuron repair after CIS damage.