Unveiling the Anticancer Mechanisms of Prodigiosin by Inhibiting of CDK1, TOP2A, and AURKB Expression in Cervical Carcinoma
Received Date: Aug 03, 2024 / Published Date: Aug 19, 2025
Abstract
Prodigiosin (PG) demonstrates a selective targeting effect on tumor cells. However, its role in cervical carcinoma is still being studied. In this study, we aim to study the specific targets and mechanism of PG in cervical carcinoma. We employed GO enrichment and KEGG analysis to unravel gene functions in CC patients, and performed differential gene expression analysis to identify core genes. To corroborate the expression levels of these core genes, we used tissue staining and RT-PCR on both normal and tumor tissues. Following this, the specific effects of PG on Hela, H8, and A549 cells were compared. After PG treatment, cell viability was evaluated using a CCK8 assay at various PG concentrations. Apoptosis in Hela cells was determined through flow cytometry post-PG treatment, and the expression of target genes was measured via RT-PCR. Our results highlighted CDK1, TOP2A, and AURKB emerging as core genes. The expression of CDK1, TOP2A, and AURKB, both at the protein and gene levels, was found to be higher in cervical carcinoma tissues compared to controls, corroborating our database analysis results. Furthermore, lower PG concentrations diminished the viability of Hela and A549 cells without significantly impacting H8 cells. PG was observed to induce apoptosis in Hela cells while simultaneously reducing the expression of CDK1, TOP2A, and AURKB genes. In summary, CDK1, TOP2A, and AURKB may significantly influence the progression and prognosis of CC. Moreover, these genes seemingly play a pivotal role in the apoptosis of cervical carcinoma cells induced by PG.
Keywords: Prodigiosin, Cervical carcinoma, Gene expression omnibus, Bioinformatics
Citation: Zhu Z, Chen Q, Tang M, Xing H (2025) Unveiling the Anticancer Mechanisms of Prodigiosin by inhibiting of CDK1, TOP2A, and AURKB Expression in Cervical Carcinoma. Diagnos Pathol Open 10: 256.
Copyright: 漏 2025 Zhu Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
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