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

机译:基于mRNA表达谱和预测的microRNA相互作用探索宫颈癌的分子机制

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摘要

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 (CHEK1), SRY-box 17 (SOX17), centrosomal protein 55, cyclin dependent kinase inhibitor 2A (CDKN2A), 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 SOX17 is associated with the regulation of embryonic development, the determination of cell fate and likely promotes cancer cell transformation. The dysregulation of CHEK1 and CDKN2A 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.
机译:宫颈癌的分子机制已通过多组学数据进行了最少的探索。在本研究中,mRNA表达谱进行了分析,并与预测的miRNA相互作用相结合,有助于表征宫颈癌的潜在调控机制。通过与29个正常样品进行比较,在33个肿瘤样品中总共鉴定出92个显着差异表达的基因(DEG)。 mRNA-miRNA相互作用网络分析显示,在92个DEG中有16个,包括检查点激酶1(CHEK1),SRY-box 17(SOX17),中心体蛋白55,细胞周期蛋白依赖性激酶抑制剂2A(CDKN2A)和DNA结合抑制剂4是先前报道的参与宫颈癌调控的4个miRNA的靶标。根据16个DEG的表达,可以将肿瘤和正常样品分为两类。此外,使用SurvExpress数据库进行的生存分析表明,这16个DEG可以分别显着区分低危和高危宫颈癌组。总体而言,基于针对DEGs鉴定的途径和功能富集,多种生物学过程可能参与宫颈癌的进展。 SOX17的失调与胚胎发育的调控,细胞命运的确定有关,并可能促进癌细胞的转化。 CHEK1和CDKN2A的失调可通过影响细胞周期检查点来响应DNA损伤,从而进一步促进癌细胞的增殖。与宫颈癌相关的关键基因的鉴定和生物学过程可能有助于探索分子机制。

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