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Optimization and Corroboration of the Regulatory Pathway of p42.3 Protein in the Pathogenesis of Gastric Carcinoma

机译:胃癌发病机制中p42.3蛋白调控途径的优化与确证

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摘要

Aims. To optimize and verify the regulatory pathway of p42.3 in the pathogenesis of gastric carcinoma (GC) by intelligent algorithm. Methods. Bioinformatics methods were used to analyze the features of structural domain in p42.3 protein. Proteins with the same domains and similar functions to p42.3 were screened out for reference. The possible regulatory pathway of p42.3 was established by integrating the acting pathways of these proteins. Then, the similarity between the reference proteins and p42.3 protein was figured out by multiparameter weighted summation method. The calculation result was taken as the prior probability of the initial node in Bayesian network. Besides, the probability of occurrence in different pathways was calculated by conditional probability formula, and the one with the maximum probability was regarded as the most possible pathway of p42.3. Finally, molecular biological experiments were conducted to prove it. Results. In Bayesian network of p42.3, probability of the acting pathway “S100A11→RAGE→P38→MAPK→Microtubule-associated protein→Spindle protein→Centromere protein→Cell proliferation” was the biggest, and it was also validated by biological experiments. Conclusions. The possibly important role of p42.3 in the occurrence of gastric carcinoma was verified by theoretical analysis and preliminary test, helping in studying the relationship between p42.3 and gastric carcinoma.
机译:目的通过智能算法优化和验证p42.3在胃癌(GC)发病机理中的调控途径。方法。利用生物信息学方法分析p42.3蛋白的结构域特征。筛选出具有与p42.3相同结构域和相似功能的蛋白质,以供参考。通过整合这些蛋白质的作用途径,建立了可能的p42.3调控途径。然后,通过多参数加权求和法求出参考蛋白与p42.3蛋白的相似性。计算结果作为贝叶斯网络中初始节点的先验概率。此外,通过条件概率公式计算出不同途径发生的概率,将概率最大的途径视为p42.3的最可能途径。最后,进行了分子生物学实验证明。结果。在p42.3的贝叶斯网络中,作用途径“ S100A11→RAGE→P38→MAPK→微管相关蛋白→纺锤体蛋白→着丝粒蛋白→细胞增殖”的可能性最大,并通过生物学实验进行了验证。结论。理论分析和初步试验证实了p42.3在胃癌发生中的重要作用,有助于研究p42.3与胃癌的关系。

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