Exploration of the molecular mechanisms of cervical cancer based on mRNA expression profiles and predicted microRNA interactions

• Published in: Oncology letters Vol. 15; no. 6; pp. 8965 - 8972
• Main Authors: Zhao, Liang, Zhang, Zhechao, Lou, Hongyan, Liang, Jingjing, Yan, Xiaojian, Li, Wenfeng, Xu, Yunsheng, Ou, Rongying
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.06.2018; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Annotations; Care and treatment; Cell cycle; Cell division; Cervical cancer; Datasets; Development and progression; Encyclopedias; Gene expression; Genetic aspects; Genomes; Health aspects; Human papillomavirus; Kinases; Medical screening; Messenger RNA; Metastasis; MicroRNA; Oncology; Ontology; Proteins; differentially expressed genes; microRNA; survival analysis; cervical cancer
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2018.8494

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.