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MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.

ABSTRACT: Background: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells. Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial-mesenchymal transition-related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells. Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial-mesenchymal transition, and hastening apoptosis of SNSCC cells. Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.

SUBMITTER: Cui X

PROVIDER: S-EPMC8791623 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveIn the present study, we tried to describe the role of miR-29c-3p in esophageal carcinoma (EC) and the relationship of miR-29c-3p with CCNA2 as well as cell cycle, accordingly revealing the potential molecular mechanism across cell proliferation, migration and invasion.MethodsExpression profiles of EC miRNAs and matched clinical data were accessed from TCGA database for differential and survival analyses. Bioinformatics databases were employed to predict the downstream targets of the potential miRNA, and enrichment analysis was performed on the miRNA and corresponding target gene using GSEA software. qRT-PCR was conducted to detect the expression levels of miR-29c-3p and CCNA2 mRNA in EC tissues and cells, and Western blot was performed for the examination of CCNA2, CDK1 and p53 protein levels. Subsequently, cells were harvested for MTT, Transwell as well as flow cytometry assays to examine cell viability, migration, invasion and cell cycle. Dual-luciferase reporter gene assay and RIP were carried out to further investigate and verify the targeted relationship between miR-29c-3p and CCNA2.ResultsMiR-29c-3p was shown to be significantly down-regulated in EC tissues and able to predict poor prognosis. CCNA2 was found to be a downstream target of miR-29c-3p and mainly enriched in cell cycle and p53 signaling pathway, whereas miR-29c-3p was remarkably activated in cell cycle. MiR-29c-3p overexpression inhibited cell proliferation, migration and invasion, as well as arrested cells in G0/G1 phase. As suggested by dual-luciferase reporter gene assay and RIP, CCNA2 was under the regulation of miR-29c-3p, and the negative correlation between the two genes was verified. Silencing CCNA2 could suppress cell proliferation, migration and invasion, as well as activate p53 pathway, even was seen to reverse the inhibitory effect of PFTβ on p53. Besides, in the presence of low miR-29c-3p, CCNA2 was up-regulated while p53 was simultaneously inhibited, resulting in the promotion of cell migration, invasion and cell cycle arrest.ConclusionMiR-29c-3p plays a regulatory role in EC tumorigenesis and development. MiR-29c-3p can target CCNA2 to mediate p53 signaling pathway, finally attributing to the inhibition of cell proliferation, migration and invasion, and making cells arrest in G0/G1 phase.

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MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.

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