American journal of translational research · 2022
PPIB-regulated alternative splicing of cell cycle genes contributes to the regulation of cell proliferation.
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Zhang Yuan, Liu Lei, Zhou Minghui, Zhang Yujie, Su Hongxia, Dong Dong, Wang Jia
Аннотация
BACKGROUND: Peptidylprolyl cis-trans isomerase B (PPIB) plays an important role in the process of inflammation through binding RNA, but the molecular pathogenesis is not yet clearly understood. The objective of this study was to investigate and verify the PPIB-regulated gene expressions and alternative splicing in Hela cells.
METHODS: We examined the PPIB-regulated transcriptomes in HeLa cells using RNA-seq data. Differentially expressed genes, alternative splicing analysis were carried out. Functional enrichment analysis was used to define the enrichment of each term.
RESULTS: We found that PPIB knockdown successfully downregulated PPIB in Hela cells, which promoted cell proliferation (P < 0.001), but no significant effect on cell apoptosis. Ten alternative splicing genes regulated by PPIB were detected in Hela cells. The ten top Gene Ontology biological process analysis and functional pathways of the alternative splicing genes were screened and identified. The pathways where differentially expressed genes are most enriched were toll-like receptor 4 signaling pathways and other signaling pathways relating to inflammation and immune response. In addition, PPIB affects the alternative splicing of multiple genes, and the Gene Ontology-biological process analysis showed that genes significantly related to alternative splicing changes were mainly enriched in the cell cycle (P < 0.05).
CONCLUSION: PPIB regulates the alternative splicing of cell cycle-related genes to affect cell proliferation and regulate the occurrence and development of chronic inflammatory diseases such as Nasal polyps.
METHODS: We examined the PPIB-regulated transcriptomes in HeLa cells using RNA-seq data. Differentially expressed genes, alternative splicing analysis were carried out. Functional enrichment analysis was used to define the enrichment of each term.
RESULTS: We found that PPIB knockdown successfully downregulated PPIB in Hela cells, which promoted cell proliferation (P < 0.001), but no significant effect on cell apoptosis. Ten alternative splicing genes regulated by PPIB were detected in Hela cells. The ten top Gene Ontology biological process analysis and functional pathways of the alternative splicing genes were screened and identified. The pathways where differentially expressed genes are most enriched were toll-like receptor 4 signaling pathways and other signaling pathways relating to inflammation and immune response. In addition, PPIB affects the alternative splicing of multiple genes, and the Gene Ontology-biological process analysis showed that genes significantly related to alternative splicing changes were mainly enriched in the cell cycle (P < 0.05).
CONCLUSION: PPIB regulates the alternative splicing of cell cycle-related genes to affect cell proliferation and regulate the occurrence and development of chronic inflammatory diseases such as Nasal polyps.