Zhao Liang, Zhang Zhechao, Lou Hongyan, Liang Jingjing, Yan Xiaojian, Li Wenfeng, Xu Yunsheng, Ou Rongying
Laboratory for Advanced Interdisciplinary Research, Institute of Translational Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Division of PET/CT, Department of Radiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Oncol Lett. 2018 Jun;15(6):8965-8972. doi: 10.3892/ol.2018.8494. Epub 2018 Apr 13.
The molecular mechanisms of cervical cancer have been minimally explored with multi-omics data. In the present study, mRNA expression profiles were analyzed and combined with predicted miRNA interactions to contribute to the characterization of the underlying regulatory mechanisms of cervical cancer. A total of 92 significantly differentially expressed genes (DEGs) were identified in 33 tumor samples by comparison with 29 normal samples. mRNA-miRNA interaction network analysis revealed that 16 out of the 92 DEGs, including checkpoint kinase 1 (), SRY-box 17 (), centrosomal protein 55, cyclin dependent kinase inhibitor 2A (), and inhibitor of DNA binding 4, were the targets of 4 miRNAs which were previously reported to be involved in the regulation of cervical cancer. Tumor and normal samples could be distinctly classified into two groups based on the expression of the 16 DEGs. Furthermore, survival analysis using the SurvExpress database indicated that the 16 DEGs could individually significantly differentiate low- and high-risk cervical cancer groups. Overall, multiple biological processes are likely to participate in the progression of cervical cancer based on the pathway and function enrichment identified for the DEGs. The dysregulation of is associated with the regulation of embryonic development, the determination of cell fate and likely promotes cancer cell transformation. The dysregulation of and further promote cancer cell proliferation by affecting the cell cycle checkpoint in response to DNA damage. The identification of critical genes and biological processes associated with cervical cancer may be beneficial for the exploration of the molecular mechanisms.
宫颈癌的分子机制在多组学数据研究中探索较少。在本研究中，分析了mRNA表达谱，并结合预测的miRNA相互作用，以有助于表征宫颈癌潜在的调控机制。通过与29个正常样本比较，在33个肿瘤样本中总共鉴定出92个显著差异表达基因（DEG）。mRNA-miRNA相互作用网络分析显示，92个DEG中的16个，包括检查点激酶1（）、SRY盒17（）、中心体蛋白55、细胞周期蛋白依赖性激酶抑制剂2A（）和DNA结合抑制剂4，是先前报道参与宫颈癌调控的4种miRNA的靶标。基于这16个DEG的表达，肿瘤样本和正常样本可明显分为两组。此外，使用SurvExpress数据库进行的生存分析表明，这16个DEG可分别显著区分低风险和高风险宫颈癌组。总体而言，基于对DEG的通路和功能富集分析，多种生物学过程可能参与宫颈癌的进展。的失调与胚胎发育调控、细胞命运决定相关，可能促进癌细胞转化。和的失调通过影响DNA损伤时的细胞周期检查点进一步促进癌细胞增殖。鉴定与宫颈癌相关的关键基因和生物学过程可能有助于探索其分子机制。
