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- Title
Construction and analysis of the regulatory network disturbed by the silenced Sp1 transcription factor in HeLa cells.
- Authors
Fengyan Li; Lijun Yu; Li Li; Meiyan Wei; Li, Fengyan; Yu, Lijun; Li, Li; Wei, Meiyan
- Abstract
<bold>Background: </bold>The objective of our study was to explore the characteristics of the regulatory network after siRNA-Sp1 (Specificity Protein 1) treatment in HeLa cells through the regulation network construction with bioinformatics methods.<bold>Materials and Methods: </bold>Using GSE37935 datasets downloaded from Gene Expression Omnibus data, the differentially expressed genes (DEGs) were screened out by the limma package in R software. Combining the DEGs with the data from the microRNA (miRNA) databases and transcription factor databases, an integrated regulatory network was established with Cytoscape. Then the motifs in the network were examined by FANMOD.<bold>Results: </bold>A total of 708 DEGs were screened, and a regulatory network consisting of 585 nodes and 1070 edges was constructed. By analyzing the two modules extracted from the network, we found that the most significant biological processes were cell cycle and apoptosis, some significant DEGs among them were CDKN1A, CUL5, and EGFR. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis discovered that DEGs, including EGFR, CDKN1A, RRM2B, and GADD45B, were significantly enriched in glioma pathway and p53 signaling pathway.<bold>Conclusion: </bold>While Sp1 was silenced by siRNA, the regulatory network in HeLa cells changed a lot. Genes related to cell cycle and apoptosis in the cell nucleus were dysregulated and the p53 signaling pathway was disturbed.
- Subjects
TRANSCRIPTION factor Sp1; SMALL interfering RNA; HELA cells; BIOINFORMATICS; GENE expression; MICRORNA genetics; HUMAN cell cycle; CELLS; CELLULAR signal transduction; DATABASES; GENES; MOLECULAR structure; PROTEINS; RNA; GENE expression profiling; CHEMICAL inhibitors
- Publication
Journal of Cancer Research & Therapeutics, 2015, Vol 11, Issue 4, p887
- ISSN
0973-1482
- Publication type
journal article
- DOI
10.4103/0973-1482.140811